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VII.- THE FACIAL NERVE
ANATOMY:
(A) The Nuclear and Intranuclear Pathway (L.M.N.):
The motor nucleus of the facial nerve is located in the ventral part of the tegmentum of
the pons near the midline. Fibres originating from this nucleus pass backwards in the
pons forming a loop around the sixth nerve nucleus, then emerge from the lateral
surface of the pons. The facial nerve, nervus intermedius and 8th nerve pass together
from the pons to the internal acoustic meatus. The facial nerve passes through the
facial canal in the petrous portion of the temporal bone. It emerges to the face through
the stylomastoid for amen.
At the angle of the facial canal, the nerve expands to form the geniculate ganglion which
gives the nervus intermedius that ends in the nucleus of the tractus solitarius and the
greater and lesser superficial petrosal nerves. During its course within the facial canal,
the facial nerve gives the nerve to stapedius muscle and the chorda tympani. The latter
emerges from the skull through the anterior canaliculus for the chorda tympani to join the
lingual nerve which is a branch of the mandibular division of the fifth nerve. After
emerging from the stylomastoid foramen the facial nerve gives branches to: the
stylohyoid muscle, the posterior belly of the digastric and the occipital belly of the
occipitofrontalis. It then divides within the parotid gland into 2 main branches;
1. Temporofacial: supplying the frontalis, orbicularis oculi and zygomatic muscles.
2. Cervicofacial: to the orbicularis oris, buccinator and platysma.
Cerebral cortex
The corticobulbar projections to the motor
nucleus of the facial nerve. The shaded areas in
the nuclei control muscles of the lower twothirds of the face. The nonshaded areas control
the muscles of the upper one-third of the face.
The muscles of the lower two-thirds are under
only contralateral control of the cerebral
cortex, whereas the muscles of the upper onethird are under bilateral control of the
cerebral cortex.
Motor Nucleus
of the Facial
NerVe
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Cortico-bulbar fibres (U.M.N.) to the facial nucleus
(B) The Supranuclear Pathway (U.M.N.):
1 . Corticospinal fibres : for voluntary facial movements, originate in the lower part of
the motor cortex, descend in the corona radiata, genu of the internal capsule,
cerebral peduncle, to the pons, where they decussate to supply the whole facial
nucleus of the opposite side. The superior part of each facial nucleus (innervating
the upper half of the face) receives additional supranuclear fibres from the ipsilateral
pyramidal tract.
2 . Mimic fibres : for emotional and associative movements of the face, arise from the
extrapyramidal system and reach the facial nuclei in the pons.
Functions of the Facial Nerve : 1. Motor to the following muscles:
(i) Occipitofrontalis.
(ii) Orbicularis oculi.
(iii) Orbicularis oris.
(iv) Buccinator.
(v) Stylohyoid.
(vi) Stapedius.
(vii) Platysma.
(viii) Posterior belly of the digastric.
2 . Secretory to the submaxillary and sublingual salivary glands (by the chorda tympani)
and to the lacrimal glands (by the superficial petrosal nerve).
3 . Sensations of the external auditory meatus and pre- auricular area.
4 . Proprioceptive sensations from the facial muscles.
5 . Taste sensation from the anterior 2 thirds of the tongue (by the chorda tympani).
Facial Paralysis may be due to :
1 . A supranuclear lesion affecting the pyramidal fibres.
2 . A supranuclear lesion affecting the mimic fibres concerned in emotional movements
of the face.
3 . Lower motor neurone lesions (Nuclear and infranuclear).
4 . Disorders of the facial muscles.
Causes of Bilateral Facial Pals> (Facial Diplegia): 1.
Congenital absence of facial nuclei.
2 . Polyneuritis : e.g. alcoholic, diphtheritic, leprotic, diabetic and acute infective
polyneuritis.
3 . Pontine lesions e.g. basilar artery thrombosis, brain - stem encephalitis,pontine
tumour,...etc.
4 . Bilateral otitis media.
5 . Syphilitic basal meningitis and carcinomatous meningitis.
6 . Uveoparotid syndrome of sarcoidosis.
7 . Double Bell's palsy.
BELL'S PALSY
Definition : A lower motor neurone facial palsy of acute onset due to non-suppurative
inflammation of the seventh nerve within the stylomastoid foramen.
Aetiology:
(i) Age : any age from infancy to old age, commonest in young adults.
(ii) Sex: Males are affected more than females.
(iii) Exposure to cold or air draft.
(iv) May follow acute infection of the nasopharynx.
(v) Few cases are due to the virus of herpes zoster.
(vi) Rheumatic interstitial neuritis of the facial nerve.
(vii) Perineuritis or periostitis with oedema compressing the nerve.
(viii) Ischaemic paralysis secondary to oedema.
Clinical picture:
* Usually unilateral, very rarely bilateral.
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* Onset is sudden, with pain within the ear, in the mastoid region, or around the angle of
the jaw.
* Paralysis affects both upper and lower facial muscles where voluntary, emotional and
associated movements are paralysed.
* Drooping of the eyebrow with inability to raise it.
* Obliteration of the wrinkles of the forehead.
* Wider palpebral fissure on the affected side.
* Inability to close the eye with upward rolling of the eyeball on trying to do so
(Negro's sign or Bell's phenomenon).
* Eversion of the lower lid with tearing.
* Obliteration of the nasolabial furrow.
* Deviation of the angle of the mouth to the sound side.
* Inability to retract the angle of the mouth and to whistle.
* The cheek puffs out in respiration and on blowing.
* Accumulation of food between the teeth and the cheek.
* Involvement of the chorda tympani may occur and produces loss of taste on the
anterior 2 thirds of the tongue.
* Involvement of the nerve to stapedius may occur resulting in hyperacusis
* Reaction of degeneration may occur.
* EMG of the facial muscles & facial nerve conduction studies help in diagnosis &
follow up.
Differential Diagnosis:
Bell's palsy should be distinguished from :
1. Facial palsy due to pontine lesions :5,6,7th nerve palsies + long tracts.
2 . Lesions in the posterior fossa: 8th nerve is usually involved.
3 . Facial palsy secondary to otitis media: Evidence of otitis media with ear discharge.
4 . Multiple sclerosis (M.S.)
5 . Syphilis.
6 . Facioplegic migraine: recurrent facial palsy + migrainous headache.
Prognosis:
1. Complete recovery occurs in a good percentage of cases within few weeks.
2 . Contracture may develop in the paralysed muscles.
3 . Clonic facial spasm may occur due to partial recovery.
4 . The crocodile tears syndrome: Unilateral lacrimation on eating due to regenerating
facial nerve fibres to the lacrimal gland.
5 . Recurrent facial palsy is rare.
Treatment:
(A) Medical:
1. Hot fomentation, short wave therapy and massage.
2 . Galvanic stimulation of the paralysed muscles.
3 . Corticosteroids, or A.C.T.H. are helpful if given early.
4 . Other drugs e.g. salicylates, Bl, B12 and B complex.
5 . Adhesive strapping above and below the mouth on the paralysed side to prevent
deviation of the mouth to the sound side.
(B) Surgical:
1. Decompression of the facial canal and incision of the nerve sheath.
2 . AutografL
3 . Plastic surgery to correct facial asymmetry.
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Differential Diagnosis Between Upper and
Lower Motor Neurone Facial Palsy
Panriysfe of 0w Face
Bilateral Facial Paralysis—Bell's Phenomenon
Facial nerve nucleus
Petrous bone
Fifth nerve gangli
Maxillary division
Lacrimal gland
The facial nerve.
Geniculate gangl
of facial nerve
Lingual
Branches to
facial muscles
nerve
and platysma
Cervical branch
of facial nerve
-THE AUDITORY (VESTIBULOCOCHLEAR) NERVE
Anatomy : It consists of 2 divisions:
(A) The cochlear (concerned in hearing), &
(B ) The vestibular nerve (concerned in equilibrium and postural functions)
(A) THE COCHLEAR NERVE :
Its fibres originate from the cochlea, pass in the 8th nerve within the internal acoustic
meatus across the posterior fossa crossing the cerebellopontine angle lateral to the
facial nerve, from which it is separated by the nervus intermedius. They enter t he
lateral aspect of the lower border of the pons to end in the cochlear nucleus, which
gives fibres that cross to the opposite side by 2 alternative pathways; (/) Fibres from
the dorsal part of the nucleus cross beneath the floor of the fourth
ventricle forming the striae acousticae.
(ii) Fibres from the ventral part of the nucleus enter the olive of the ipsilateral side,
which gives new fibres that cross in the ventral part of the pons as ti\Q fibres of the
trapezium.
Both dorsal and ventral fibres ascend in the lateral lemniscus to the inferior
colliculus and the medial geniculate body, from which new fibres pass to the
cortical auditory centre in the posterior part of the superior temporal gyrus.
Lesions of the Cochlear Nerve result in :
1. Tinnitus.
2 . Deafness.
(B) THE VESTIBULAR NERVE :
Its fibres arise from the Labyrinth (semicircular canals, utricle and saccule). It joins the
cochlear nerve in the internal meatus crossing the cerebellopontine angle to ente r the
pons. Its fibres end in a number of nuclei in the brain-stem. Some fibres go to the eye
muscles, others run to the cerebellum, thalamus and to the cortical centres in the
posterior parts of the temporal lobes.
Lesions of the Vestibular Nerve result in :
1. Vertigo.
2 . Spontaneous Nystagmus.
3 . Ipsilateral incoordination of limbs.
Causes of Tinnitus:
1
2
4
5
. Wax in the external acoustic meatus .
. Catarrh of the Eustachian tube.
3 . Acute otitis media.
. Forcible contraction of the orbicularis oculi.
. Drugs e.g. quinine, salicylates, amyl nitrite and streptomycin (tinnitus precedes the
deafness caused by the latter drug).
6 . Acute labyrinthitis.
7 . Arteriosclerosis.
8 . Anaemia.
9 . Aortic incontinence.
10 . Otosclerosis
11 . Carotid - cavernous sinus aneurysm, congenital I.C. aneurysm, arterial angioma may
be heard by the patient as rhythmical bruit.
12 . Acoustic neuroma.
13 . Syphilitic meningitis involving the 8th nerve.
14 . Vascular lesions of the pons may cause tinnitus and deafness.
15 . Irritative lesions of the auditory cortex e.g. temporal lobe tumours produce auditory
hallucinations.
16 . Endogenous depression.
Treatment of Tinnitus:
(i) Treat the cause.
(ii) Sedatives e.g. phenobarbitone. (MI ) Antidepressants. (iv)
Destruction of the cochlea or division of the 8th nerve in severe cases with
intolerable tinnitus.
Causes of Nerve Deafness :
1 . Lesions of the internal ear e.g. trauma, chronic otitis interna, acute labyrinthitis,
meningococcal meningitis, mumps, congenital syphilis, cogenital deaf mutism,
Otosclerosis and atheroma.
2 . Toxic e.g. streptomycin, neomycin, aspirin, quinine, tobacco, & alcohol.
3 . Traumatic e.g. fractures of the skull involving the petrous temporal bone, & chronic
exposure to loud noise.
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4 . Acoustic neuroma.
5 . Intratemporal epidermoid.
6 . Paget's disease (osteitis deformans).
7 . Meningovascular syphilis.
8 . Other causes: e.g. polyneuritis cranialis and avitaminosis.
9 . Vascular lesions of the pons.
10 . Multiple sclerosis (M.S.)
11. Tumours of the midbrain or pineal body.
12 . Bilateral temporal lobe lesions. 13
. Birth injury, anoxia and kernicterus.
VERTIGO
Definition : It is the consciousness of disordered orientation of the body in space, i.e. a
sense of rotation of the patient or of his surroundings.
Causes of Vertigo:
1. Psychogenic Vertigo (Giddiness) e.g. in hysteria and anxiety neurosis.
2 . Vertigo due to Cortical Disturbance: e.g. aura of a temporal lobe epilepsy, basilar artery migraine and intracranial tumour.
3 . Ocular Vertigo : e.g. giddiness at heights and in patients with squint(external ophthalmoplegia).
4 . Cerebellar Vertigo : e.g. in lesions of the flocculonodular lobe, intracerebellar haemorrhage and at the onset of posterior inferior cerebellar artery thrombosis.
5 . Brain-stem lesions e.g. vascular or neoplastic lesions, M.S., syringobulbia, streptomycin therapy and transient brain-stem ischaemia evoked by head movement in patients with vertebral artery atheroma and cervical spondylosis (Vertebro-basilar insufficiency).
6 . Vestibular Neuronitis may cause paroxysmal vertigo not associated with tinnitus or
deafness.
7 . Epidemic Vertigo: may be due to a mild brain-stem encephalitis.
8 . Auditory nerve lesions e.g. acoustic neuroma and basal meningitis.
9 . Aural Vertigo : e.g.
(i) Wax in the external meatus.
(ii) Blockage of the Eustachian tube.
(iii) Otitis media (acute and chronic).
(iv) Otosclerosis.
(v) Ischaemia due to atheroma, anaemia and incraesed IC T.
(vi) Herpes zoster of the geniculate ganglion.
(vii) Acute virus labyrinthitis.
(viii) Motion Sickness.
(ix) Meniere's syndrome.
(x) Drugs e.g. quinine and salicylates.
(xi) Head injury.
(xii) Benign positional vertigo.
MENIERE'S SYNDROME
Aetiology: is unknown.
* Age: middle age
* Sex: males more than females(3:2)
* Septic foci in the teeth ; tonsils or nasal sinuses .
* Association with migraine.
* Allergy.
Clinically:
1. Progressive deafness and tinnitus .
2. Recurrent attacks of vertigo
3 . Nausea, vomiting , prostraion and diplopia.
4 . Unsteadiness and staggering
5 . Rotary nystagmus .
Treatment:
(A) Medical
(i) Rest during the attack .
(ii) Chlorpromazine , 50 mg.i.m.
(iii) Phenobarbitone.
(iv) Antihistaminics.
(v) Vasodilators.
(vi) Eradication of any septic foci,
(vii) Salt-free diet with restricted fluid intake, (viii) Diuretics.
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Vestibuiar nuclei \
Dorsal cochlear nerve \
Utricle Ampulla of
semicircular canal
The acoustic nerve and its connections
Temporal
lobe of
cerebral
cortex
Dorsal cochlear
nucleus
Inferior cerebellar
peduncle
Ventral cochlear
nucleus
Cochlear
nerve
entering at level of
upper medulla
Superior olivary
nucleus
Trapezoid body
The auditory system. The important point to observe is that this system is represented
bilaterally in the cerebral cortex
Auricular br. of vagus
Tympanic branch
Spinal part of accessory nerve
Glossopharyngeal nerve
Pharyrigeal nerve
Recurrent laryngeal nerve
Sup. laryngeal nerve
The Glossopharyngeal, Vagus & Accessory Nerves
Taste
|
General Sensation
Sensovy Innervation of the Tongue
(B) Surgical:
(i) Dividing the vestibular nerve.
(iii) Endolymphatic subarachnoid shunt.
(ii) Ultrasonic irradiation,
(iv) Removal of the utricle.
IX. - THE GLOSSOPHARYNGEAL NERVE
Anatomy:
1 . Sensory fibres : end in the nucleus of the tractus solitarius and the dorsal nucleus of
the vagus. They carry sensations from the posterior third of the tongue, the tonsils
and the pharynx.
2 . Taste fibres : end in the dorsal nucleus of the nerve in the medulla which gives fibres
to the thalamus and then to the lowermost part of the sensory cortex. They convey
taste from the posterior third of the tongue.
3 . Secetory fibres to the parotid gland.
4 . Motor fibres : arise in the inferior salivary nucleus and in the nucleus ambiguus. They
supply the stylopharyngeus muscle.
The 9th nerve crosses the posterior fossa, emerges through the jugular foramen to
descend in the neck between the internal carotid artery and the internal jugular vein,
then between the internal and external carotid arteries.
Glossopharyngeal Neuralgia:
It resembles trigeminal neuralgia, but pain starts in the tonsillar fossa, back of throat and
larynx and may radiate to the ipsilateral ear. It is precipitated by swallowing or by
protruding the tongue . Its cause is unknown. Treatment:
(1) Carbamazepine (Tegretol) 200 mg. t.d.s.
(2) Surgical division of the affected nerve in the posterior fossa.
TASTE SENSATION
Four tastes are known :
(i) Sweet
(ii) Salt
(iii) Bitter, and
(iv) Acid.
Pathways:
"
*.
1 . Taste fibres from the anterior 2 thirds of the tongue pass in the lingual nerve —>
Chorda tympani -> facial nerve —> geniculate ganglion —» nervus intermedius ->
pons.
2 . Taste fibres from the posterior third of the tongue, the pharynx and the lower border
of the soft palate are carried by the 9th nerve (glossopharyngeal).
3 . On reaching the pons, taste fibres enter the tractus solitarius —> nucleus of the tractus
solitarius -> New fibres that cross the midline -> gustatory lemniscus -> ascends to the
thalamus -> cortical centre for taste in the lowermost part of the sensory cortex. Ageusia :
Loss of taste. Causes of Ageusia:
(i) Lesions interrupting the pathways of taste fibres, (ii )
Post-traumatic ageusia: after head injury, (iii) Bilateral
thalamotomy for treatment of parkinsonism.
N.B.: Gustatory hallucinations may occur with olfactory hallucinations in irritative
lesions of the uncus.
X. - THE VAGUS NERVE
Anatomy : It consists of sensory and motor fibres. 1 .
Sensory fibres :
(i) Somatic sensory fibres : end in relation with the spinal tract of the 5th nerve and its
nucleus. They supply common sensibility to a part of the external ear. (ii) Visceral
sensory (afferent) fibres : end in the nucleus of the tractus solitarius and
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the dorsal nucleus of the vagus. They convey visceral sensations from the
pharynx, larynx; trachea, oesophagus and thoracic and abdominal viscera.
2. Motor fibres : arise from 2 nuclei in the medulla:
(i) The nucleus ambiguus : gives motor fibres to the striated muscles of the palate,
pharynx, and larynx, (ii) The dorsal nucleus of the vagus : gives fibres to the
parasympathetic ganglia of the
vagal plexuses, innervating the thoracic and abdominal viscera.
The vagus nerve leaves the skull through the jugular foramen to enter the neck, where it
lies behind the carotid arteries and the internal jugular vein. It enters the thorax behind
the large veins. The two vagi enter the abdomen via the oesophageal opening of the
diaphragm to supply the abdominal viscera. The main branches of the vagus nerve : 1. A
meningeal branch : innervates the dura mater of the posterior fossa.
2 . An auricular branch : supplies common sensibility to the back of the auricle and
external acoustic meatus.
3 . A pharyngeal branch : supplies motor fibres through the pharyngeal plexus for the
muscles of the pharynx and soft palate except the stylopharyngeus and the tensor veli
palatini.
4 . Superior laryngeal nerve : gives two branches:
(/) The internal laryngeal branch : is the sensory nerve of the larynx. (ii) The external
laryngeal branch : innervates the inferior constrictor of the pharynx and the
cricothyroid muscles.
5 . Cardiac branches.
6 . Recurrent laryngeal nerves (Rt & Lt): innervate all the muscles of the larynx (except
the cricothyroid muscles) and also innervate the cricopharyngeus muscles which form the
lower sphincter of the pharynx. Lesions of the Glossopharyngeal and Vagus Nerves :
1 . Unilateral pure motor paralysis :
Poliomyelitis, diphtheria and botulism.
2 . Unilateral motor paralysis and sensory loss:
Syringobulbia, vascular lesions in the medulla, posterior fossa tumours, trauma,
tumours or enlarged glands at the jugular foramen .
3 . Bilateral C/.MJV. paralysis :
* Double stroke (pseudobulbar palsy).
* Motor neurone disease.
4 . Bilateral L.M.N. paralysis :
* Poliomyelitis.
* Progressive bulbar palsy .
* Diphtheria and botulism
5 . Fatiguable motor paralysis : Myasthenia gravis .
6 . Palatal nystagmus : (Constant rhythmic vertical oscillation of the palate) e.g. due to a
vascular lesion involving the central tegmental tract.
CLINICALLY:
(A) Lesions of the Glossopharyngeal Nerve (9th): result in :
(/ ) Loss of taste and anaesthesia over the posterior third of the tongue. (ii) Sensory
loss of the upper part of the pharynx with loss of the pharyngeal reflex (gag reflex).
(B) Lesions of the Vagus Nerve (10th): result in :
(/) Paralysis of the soft palate -> nasal speech and nasal regurgitation.
(11) Paralysis of the pharynx —> dysphagia .
(MI ) Paralysis of the larynx -* hoarseness of voice (total unilateral paralysis of one
vocal cord) or aphonia (bilateral total paralysis of the vocal cords, both being
immobile in mid-abduction), (iv) Loss of palatal and
pharyngeal reflexes (gag reflex).
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(C) Lesions of the Recurrent Laryngeal Nerve :
(i) Unilateral: e.g. Mediastinum syndrome, enlarged cervical glands, cancer thyroid
and operations on the neck . * This will result in unilateral abductor paralysis of one
vocal cord,which remains in
the midline. (ii) Bilateral: e.g. Enlarged cervical glands, goitre and trauma.
This will produce
bilateral abductor paralysis of the vocal cords, where both cords lie adducted
together and are immobile on inspiration leading to respiratory obstruction.
NB.: In unilateral palatal paralysis, the palate and uvula move up towards the normal side
on phonation. Also in unilateral pharyngeal paralysis, the pharyngeal muscles move
towards the normal side on phonation (curtain movement).
XL -THE ACCESSORY NERVE
Anatomy:
* It is a purely motor nerve.
* It consists of two portions :
1, The cranial portion arises from the nucleus ambiguus of the medulla, arises from the
2, The spinal portion anterior horn cells of the upper five cervical segments of the
spinal cord. It ascends to enter the skull through the
foramen magnum, joins the cranial portion to leave the skull through the jugular
foramen, where the cranial portion joins the vagus to supply the pharynx and larynx.
The spinal portion descends in the neck between the internal carotid artery and the
internal jugular vein, to supply the sternomastoid and trapezius muscles. Lesions : may be .
(a) Nuclear : e.g. poliomyelitis, motor neurone disease, polyneuritis, syringobulbia and
tumours.
(b) Infranuclear : e.g. tumours, syphilis, otitis media, cervical lymphadenitis,
operations in the neck, polyneuritis, myasthenia gravis, myotonia atrophica and
polymyositis.
Clinically:
1 . A unilateral lesion : causes ipsilateral paresis or paralysis of the sternomastoid and
upper part of the trapezius.
2 . A bilateral lesion : produces paralysis of both sternomastoids and both trapezii.
Paralysis of the Eleventh Cranial Nerve (Spinal Accessory)
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XIL - THE HYPOGLOSSAL NERVE
Anatomy:
* It is the motor nerve of the tongue.
* It arises from the hypoglossal nucleus of the medulla.
* Its fibres emerge from the ventral aspect of the medulla between the olive and
pyramid.
* It passes across the posterior fossa to leave the skull through the hypoglossal canal.
* It descends in the neck, reaching the tongue by passing between the mylohyoid and
hypoglossus muscles.
* It gives a descending branch that joins the descending cervical nerve to form the ansa
hypoglossis which innervates most of the infrahyoid muscles.
* It gives another branch to supply the thyrohyoid muscles.
Lesions : may be * U.M.N.L.: Unilateral or Bilateral.
* L.M.N.L.: Unilateral or Bilateral.
1. Unilateral upper motor neurone lesions : e.g.
Hemiplegia due to cerebrovascular accidents or deep - seated tumours.
2 . Bilateral U.MM.L. e.g.
* Double stroke producing pseudobulbar palsy.
* Motor neurone disease.
3 . Unilateral L.MM.L. e.g.
* Syringobulbia.
* Syphilitic meningitis.
* Poliomyelitis.
* Otitis media.
* Brain-stem angiomas or tumours.
* Periostitis of the hypoglossal canal.
* Vertebral artery thrombosis or aneurysm.
* Trauma, tumours, or enlarged glands high in the neck.
4 . Bilateral L.M.N.L. : e.g.
* Motor neurone disease
* Syringobulbia.
* Retropharyngeal abscess.
* Subluxation of the odontoid process.
* Foramen magnum anomalies such as Arnold - Chiari malformation and basilar
impression of the skull.
Paralysis of the Tongue
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Clinically:
1 . Unilateral U.MNJL. : causes deviation of the tongue to the opposite side of the lesion
(hemiplegic side) on protrusion.
2 . Bilateral U.M.N.L. : causes a small, tight, spastic tongue lying in the floor of the
mouth, with inability to protrude the tongue and dysarthria + Exaggerated jaw jerk. 3.
Unilateral L.M.N.L. : causes paralysis of the corresponding half of the tongue,
wasting with or without fasciculation and deviation of the tongue to the paralysed
side on protrusion.
4 . Bilateral L.M.N.L. rleads to bilateral paralysis, wasting and fasciculation, with
inability to protrude the tongue and dysarthria.
5 . Both UM.N.L. and L.M.N.L. may co - exist as in motor neurone disease, where
pseudo and true (progressive) bulbar palsy coexist.
Features
1 . Paralysis :
Bilateral U.M.N.L.
Spastic, tight, immobile
2 . Wasting :
tongue.
Small, tight tongue but
no actual wasting
3 . Fasciculation :
4 . Jaw Jerk
5 .R.D.:
Absent
Exaggerated.
Absent
Features
1. Paralysis:
2 . Wasting :
3. Fasciculation:
4 . Jaw Jerk
5. R.D.:
Bilateral U.M.N.L.
Spastic, tight, immobile
tongue.
Small, tight tongue but
no actual wasting
Absent
Exaggerated.
Absent
Bilateral L.M.N.L.
Flaccid immobile tongue
Wasted tongue with
exaggerated longitudinal
folds.
Present
Normal
Present
Bilateral L.M.N.L.
Flaccid immobile tongue
Wasted tongue with
exaggerated longitudinal
folds.
Present
Normal
Present
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CHAPTER 3 THE
PYRAMIDAL SYSTEM
( CORTICOSPINAL TRACT )
Anatomy:
The corticospinal (pyramidal) fibres are the axons of the Betz cells, large ordinary
pyramidal cells and simple giant cells ofBrodmann's areas 4 and 6. They descend from the
motor cortex, pass through the corona radiata to enter the internal capsule where they
occupy the posterior one third of the anterior limb, the genu, and the anterior two - thirds of
posterior limb. (The body is represented here as follows; head fibres in genu of internal
capsule followed by upper limb fibres, trunk fibres and lastly lower limb fibres from before
backwards). The pyramidal fibres reach the midbrain where they occupy the middle 3 fifths
of the crus cerebri. They enter the pons where they become broken into scattered bundles by
the transverse pontine fibres and the nuclei pontis. They reunite at the ponto - medullary
junction to form the pyramids on the anterior aspect of the medulla. At the lower end of the
medulla, each pyramidal tract divides into 3 parts :
1. The crossed pyramidal (corticospinal) tract: consists of the larger part that crosses
in the " motor decussation" to descend in the lateral column of the spinal cord on the
opposite side.
2 . The direct pyramidal (corticospinal) tract : consists of the smaller part that
descends in the anterior column of the spinal cord on the same side. Its fibres
gradually cross as they descend, ending at the mid - thoracic region.
3 . Uncrossed fibres : also remain in the lateral column, supplying the muscles of the
trunk and respiration.
All pyramidal fibres enter the grey matter of the spinal cord to end on the anterior born
cells, either directly or through internuncial fibres.
N.B.: The motor nuclei of the cranial nerves are all supplied by fibres from both pyramidal
tracts and thus controlled by both cerebral hemispheres except the inferior part of the
facial nuclei that innervates the lower half of the face, and the hypo glossal nuclei and
rarely the mandibular nerve. These are only controlled by the opposite motor cortex.
Function:
The pyramidal tracts carry the nervous impuless which initiate voluntary movements from
the motor cortex to the lower motor neurones in the brain-stem and spinal cord. Lesions:
(A) Unilateral lesions at any level above the fifth cervical segment of the spinal cord
produce Hemiplegia.
(B) Bilateral lesions:
1. In the cerebral hemispheres : produce Pseudobulbar Palsy & Mental Symptoms.
2. In the brain-stem : produce Pseudobulbar Palsy.
3 .In the spinal cord:
(a) In the cervical region : produce Quadriplegia
(b) In the thoracic region: produce Paraplegia
N .B.: The lower motor neurones (L.M.N.) consist of:
(i) The motor nuclei of the cranial nerves in the brain-stem and the anterior horn cells
of the spinal cord.
(ii) The axons of these cells pass into the cranial nerves and the ventral roots of the
spinal nerves. From the latter they pass to the peripheral nerves. Each LM.N
innervates a bundle of 150 or more muscle fibres.
64
Motor Cortex
Internal Capsule
Midbrain
Pons
Medulla
Lateral Corticospinal (crossed
pyramidal) tract
Ventral Corticospinal
(direct pyramidal) tract
Spinal Cord
The Pyramidal System
Lesion
HEMIPL
EGIA
Rotation of the head toward
the lesion
Conjugate ocular deviation toward the lesion
1
U.M.N. facial palsy
12 th nerve palsy
( Aphasia
only
occurs
with left
sided
lesions )
deviation of lower jaw toward hemiplegic side
Hemiplegic posture
Abdominal reflexes i or lost
Weakness or paralysis of one side of the body
(skilled movements are most affected )
Hemianaesthesia
Cremasteric reflex I or lost
Spasticily of clasp knife Type
Hyperreflexia
± ankle clonus
Ciicumdu
ction gait
Extensor
plantar
response
(Babinski
's sign)
U.M.N.L.
Features
L.M.N.L.
1. Paralysis or Unilateral lesions above the pyrami- Paralysis or paresis of the muscles
paresis
2. Wasting
3. Muscle tone
4. Reflexes
5. Babinski's
dal decussation produce paralysis on
the opposite side, while those below
the decussation prodyce paralysis on
the same side of the lesion
Absent (disuse atrophy may occur
after prolonged paralysis)
Hypertonia (spasticity)
Hyperreflexia (exaggerated deep
tendon jerks).
Present (extensor plantar response)
sign
6. Fasciculation Absent.
7. Trophic
Absent
changes
8. Reaction of
Degeneration
9. E.M.G.
supplied by the affected L.M.N.
Present
Hypotonia (Flaccidity)
Hyporeflexia or areflexia
Absent
May be present
Often present e.g. coldness, cyanosis and brittle nails in the paralysed limb (due to disuse and vasomotor paralysis)
Present
Absent
„
No evidence of L.M.N.L.
Evidence of L.M.N.L.
HEMIPLEGIA
DEFINITION:
Hemiplegia : means paralysis of one side of the body due to a unilateral corticospinal
(pyramidal) lesion at any level between the motor cortex and the fifth cervical segment.
Crossed hemiplegia rmeans cranial nerve palsies on one side with hemiplegia on the
contralateral side of the body. It results from brain-stem lesions.
CAUSES OF HEMIPLEGIA :
(A) Functional or Hysterical hemiplegia.
(B) Organic:
1 . Congenital: e.g. Cerebral palsy. 2.
Traumatic:
(a) Immediate post-traumatic hemiplegia may occur due to:
i. Epidural or intracerebral haemorrhage.
ii. Cerebral contusion or laceration.
(b) Delayed post-traumatic hemiplegia may occur due to :
i. Chronic subdural haematoma.
ii. Post-traumatic cerebral atrophy,
iii. Post-traumatic cicatrisation.
65
3 . Inflammatory : e.g. Meningitis, Encephalitis, Syphilis, or Brain abscess.
4 . Neoplastic: e.g. Brain tumours,
whether primary such as meningiomas
and gliomas, or metastatic.
5 . Degenerative or Demyelinating :e.g.
(a) Multiple sclerosis (M.S.).
(b) Disseminated encephalomyelitis (D.E.M.).
6. Vascular lesions : are the commonest cause
of hemiplegia. They include the following.:
(a) Cerebral Thrombosis: secondary to:
i. Disease of the vessel wall such as :
* Cerebral arteriosclerosis.
* Syphilitic endarteritis.
* Periarteritis nodosa.
ii. Disease of the blood such as :
* Polycythemia vera.
'* Profound anaemia.
Hi. Circulatory disorder such as :
* Systemic hypotension and slow circulation.
* Myocardial infarction.
Thrombotic hemiplegia usually occurs during sleep.
(b) Cerebral Embolism :The embolus may come from :
Hem/pteg/a and Hem/pares/s
i. The heart & great vessels e.g. in :
* Atheroma of the carotid, vertebral, innominate, subclavian arteries or the
aorta.
* Rheumatic heart disease, mitral stenosis and A.F.
* Bacterial endocarditis (detached vegetations).
* Congenital heart disease.
* Myocardial infarction.
ii. The Lung : e.g. in :
* Bronchogenic carcinoma (metastatic emboli).
* Suppurative lung syndrome e.g. lung abscess.
iii. Peripheral vessels e.g:
* Pelvic thrombophlebitis.
* Femoral thrombophlebitis.
iv. Other Emboli : e.g. Fat embolism, air embolism, parasitic emboli and
malignant emboli.
(c) Cerebral Haemorrhage:
i. Combination of hypertension and cerebral arteriosclerosis.
//. Ruptured intracranial aneurysm or angioma.
iii. Haemorrhagic blood disease e.g. purpura.
iv. Strain of whooping cough.
v. Head injury.
vi. Arsenical poisoning.
(d) Hypertensive encephalopathy:
Transient protective spasm of the cerebral arteries occurs in malignant hypertension and may lead to hemiplegia (temporary or permanent) due to ischaemia or
thrombosis occurring on top of spasm.
(e) Lateral sinus thrombosis : secondary to otitis media.
66
CLINICAL PICTURE:
Onset: may be:
(i) Sudden : e.g. in embolism and haemorrhage.
(ii) Rapid : e.g. in thrombosis, haemorrhage, meningitis, encephalitis and hysteria.
(iii) Gradual: e^ LahraiatiL(mur£7htaia
and hysteria.
Course rmaybe:
(i) Regressive : e.g. in vascular lesions (thrombotic and embolic) and in infective
lesions.
(ii) Progressive : e.g. in neoplastic and degenerative lesions, (iii)
Remittent : e.g. in M.S. Symptoms and Signs: I. - Motor Power
:A pyramidal lesion results in :
(A) Negative Signs : paralytic manifestations are due to loss of the corticospinal
control.
(B) Positive Signs: appearance of new phenomena e.g. muscular hypertonia and
extensor plantar response. These are release phenomena due to the liberation of intact
parts of the nervous system from the control of the pyramidal system. (A)Negative
Signs:
1. Conjugate ocular deviation towards the side of the lesion due to transitory paralysis of
centre.
2 . Rotation of the head towards the side of the lesion (transitory).
3 . Upper motor neurone facial palsy on the side of hemiplegia with paralysis of voluntary
movements of the lower part of the face, while emotional movements as smiling and
crying and associated movements as involuntary retraction of the angle of the mouth
on voluntary closure of the eyes, are spared.
4 . Deviation of the tongue towards the hemiplegic side on protrusion.
5 . Deviation of the lower jaw towards the hemiplegic side on opening the mouth, due to
paralysis of the mandibular nerve on that side.
6 . Weakness of the palatal movements on the side opposite the lesion,with deviation of the
uvula towards the lesion.
7 . Paralysis or paresis of the upper and lower limbs on the side opposite the lesion. The
finer and more skilled movements are more affected than the grosser and less skilled.
Therefore, buttoning, sewing and playing the piano become clumsy. The extensors of
the upper limb are more affected than flexors and the reverse occurs in the lower limb.
8 . Respiratory Movements : more expansion of the paralysed side of the chest occurs
during quiet breathing, but the opposite occurs during forced breathing .
9 . Circumduction Gait: Swinging the paralysed leg outwards at the hip,with extension at
the knee and plantar flexion of the foot and toes.
(B) Positive Signs:
1 . Muscular Hypertonia (Clasp Knife Spasticity ) :
Acute lesions e.g. vascular or infective are followed immediately by flaccidity of the
paralysed limbs due to neural shock. After2 or 3 weeks, gradual return of tone and
ultimately hypertonia occurs. In the upper limb : the adductors and internal rotators of
the shoulder, flexors of the elbow, wrist and fingers and the pronators of the forearm
are more spastic than their antagonists.
In the lower limb :the adductors of the hip, extensors of the hip and knee, plantar flexors of the foot and toes are more spastic than their antagonists. Contractures may
develop in the spastic muscles.
2 . Hemiplegic Posture :
Is determined by the hypertonic (spastic)muscles. So the arm is adducted and
67
internally rotated, the elbow, wrist, and fingers are flexed and the forearm is pronated,
while the lower limb is extended at the hip and knee, with plantar flexion and
inversion of the foot 3. Reflexes:
(a) Deep reflexes : are exaggerated after recovery from the shock stage and clonus may
be present.
(b) Superficial abdominal and cremasteric reflexes are diminished or lost on the
hemiplegic side.
(c) Extensor plantar response (Babinski sign) on the hemiplegic side.
II - Sensations : Hemianaesthesia on the hemiplegic side may occur due to affection of the
sensory fibres.
HI - Speech:
Aphasia or dysphasia may occur in left-sided lesions, in right-handed people.
LOCALIZATION OF LESIONS OF THE PYRAMIDAL TRACT IN HEMIPLEGIA
(A) Cortical Lesions (Cortical Hemiplegia):
1 . Monoplegia rather than hemiplegia.
2 . Cortical sensory loss in the paralysed limb occurs if the sensory cortex is involved .
3 . Jacksonian convulsions on the affected side of the body, which may become
bilateral with loss of consciousness.
4 . Aphasia may occur in left-sided lesions. 5 . Coma may occur at athe onset.
6 . Homonymous hemianopia may occur in parieto- occipital lesions.
(B) Subcortical Lesions (Subcortical Hemiplegia):
1. Hemiplegia with predominent weakness in one limb
2.Cortical hemi-anaesthesia on the hemiplegic side, due to affection of thalamo-cortical
sensory fibres. 3.Crossed homonymous hemianopia, due to involvement of the
optic radiation.
(C) Capsular Lesions (Capsular Hemiplegia):
1.Complete hemiplegia.
2. Hemianaesthesia on the hemiplegic side.
3. Homonymous hemianopia may occur. 4. No coma, convulsions or aphasia.
(D) Midbrain Lesions:
1. Weber's syndrome:
* Ipsilateral third nerve paralysis (ophthalmoplegia).
* Contralateral hemiplegia.
2. Benedikt's syndrome:
* Ipsilateral third nerve paralysis.
* Contralateral hemiplegia, hemianaesthesia and involuntary choreiform movements.
(E) Pontine Lesions:
1. Millard-Gubler's syndrome:
* Ipsilateral L. M. N. 6th and 7th nerve palsies.
* Contralateral hemiplegia.
* Ipsilateral paralysis of the jaw muscles may occur (5th nerve palsy).
2. Foville's syndrome:
* Paralysis of conjugate ocular deviation to the side of the lesion.
* Contralateral hemiplegia.
* Ipsilateral L.M.N. facial palsy may be present
* Ipsilateral paralysis of the jaw muscles may occur.
N.B.: Homer's syndrome; fifth nerve palsy (motor & touch); trigemino-thalamic tract,
spinothalamic tract, medial lemniscus & pyramidal tract affection; hyperyrexia and pinpoint puplis may occur in pontine lesions.
68
(F) Medullary Lesions (Medullary Hemiplegia):
1. Central medullary lesion : causes bilateral hemiplegia due to affection of the pyrami
dal decussation.
2. Lateral medullary lesion:
* Ipsilateral paralysis of the tongue, soft palate and vocal cord.
* Ipsilateral horner's syndrome.
* Ipsilateral trigeminal analgesia and thermo-anaesthesia.
* Ipsilateral cerebellar ataxia.
* Contralateral hemianaesthesia and hemiplegia.
(G) Spinal Hemiplegia: is due to hemisection of the spinal cord (traumatic or
extramedullary compression). It presents with the Brown-Sequard syndrome :
l.At the level of the lesion:
(a) L. M. N. paralysis due to damage of the anterior horn cells at the level of the
lesion.
(b) Loss of all sensations due to damage of the posterior horn at the site of the legion.
2. Below the level of the lesion:
(a) Motor paralysis (Hemiplegia) on the same side of the lesion (pyramidal tract
affection).
(b) Deep sensory loss on the same side of the lesion (posterior column affection).
(c) Loss of pain and temperature sensations on the opposite side (damage of the
crossed spinothalamic tract).
(d) Touch is relatively preserved on both sides.
PSEUDOBULBAR PALSY
Definition : Bilateral supranuclear paralysis of the bulbar muscles, usually associated with
emotional incontinence and/ or spastic quadriparesis due to interruption of the
corticospinal and corticobulbar tracts.
Causes:
1. Heredofamilial: e.g. Juvenile motor neurone disease.
2. Inflammatory lesions e.g. D.E.M. & G.PJ. (General paralysis of the insane).
3. Vascular lesions e.g.
(i) Double stroke (bilateral hemiplegia). (ii)
Vertebro-basilar insufficiency, (iii) Cerebral
arteriosclerosis, (iv) Syphilitic
cerebrovascular disease.
4. Demyelinating lesions: e.g. M.S.
5. Degenerative lesions e.g. M.N.D. (motor neurone disease).
6. Neoplastic lesions: e.g.: Brain-stem gliomas.
7. Idiopathic: e.g. Cortico-striato-spinal atrophy (pseudosclerosis).
Clinically:
1. Onset: is sudden in vascular lesions and gradual in neoplastic and degenerative
lesions.
2. Bulbar Manifestations (due to supranuclear lesion of the 9th, 10th and 12th cranial
nerves).
(i) Dysarthria, slurred, spastic or nasal type of speech, (ii)
Dysphagia: difficulty in swallowing, (iii) Hoarseness of voice, or
aphonia, (iv) Nasal regurgitation of fluids. No wasting or fasciculation
in the muscles of the palate and tongue.
69
3. Emotional lability or incontinence:
Bouts of uncontrolable laughing and crying of sudden onset and sudden cessation
with no logic stimulus and discrepancy between the emotional experience and
expression.
4. Exaggerated jaw jerk.
5. Quadriparesis or quadriplegia may be present.
N.B.: Progressive bulbar palsy occurs in lower motor neurone lesions of the 9th, 10th and
12th cranial nerves.
Differentiation Between Pseudobulbar and
Progressive Bulbar Palsies
Emotional lability
70
CHAPTER 4
CEREBROVASCULAR DISORDERS
BLOOD SUPPLY OF THE BRAIN
Arterial Supply of the Brain:
The brain receives its arterial blood from 2 systems: the carotid and vertebro-basilar (2
internal carotids and 2 vertebrals)
(A) The internal carotid artery is a branch of the common carotid. It enters the skull
through the carotid canal to the cavernous sinus.
It consists of 4 segments: cervical, intrapetrosal, intracavernous & supraclinoid, the last
2 segments are called carotid siphon. It gives the following main branches:
(i) the ophthalmic artery.
(ii) the posterior communicating artery.
(iii) the anterior choroidal artery.
(iv) the anterior cerebral artery and
(v) the middle cerebral artery.
The anterior cerebral artery : supplies the medial surface of the anterior 3/5 of the
cerebrum. The middle cerebral artery : supplies the lateral surface of the
anterior 3/5 of the
cerebrum.
(B) The two vertebral arteries (right and left) are branches of the subclavian arteries.
They enter the skull through the foramen magnum. They unite at the lower border of the
pons to form the basilar artery, which bifurcates at the upper border of the pons into the 2
posterior cerebral arteries (Rt. & Lt.)
Each Vertebral artery gives:
(i) a posterior spinal artery.
(iii) a posterior inferior cerebellar artery.
(ii) an anterior spinal artery.
(iv) a posterior meningeal artery.
The Basilar artery gives:
(i) the anterior inferior cerebellar artery.
(ii) the labyrinthine arteries.
(iii) Paramedian and circumferential pontine branches.
(iv) the superior cerebellar artery &
(v) the 2 posterior cerebral arteries.
The vertebrobasilar system supplies the posterior 2/5 of the cerebrum, the brain - stem,
the cerebellum and the spinal cord.
(C) The Circle of Willis: is located on the base of the brain (inferior surface). This circle is
formed by the anastomosing branches of the internal carotid arteries and the basilar artery.
These are the anterior and posterior communicating arteries, the anterior, middle and
posterior cerebral arteries.
Each of the main cerebral arteries: anterior, middle and posterior, gives two types of
branches:
(a) the central or ganglionic branches.
(b) the cortical or circumferential branches.
The Central or Ganglionic arteries: Supply the diencephalon, basal ganglia and
internal capsule Blood Supply
of the internal capsule:
(i) The striate branches of the middle cerebral artery -> the superior half of the anterior and posterior limbs of the internal capsule, (ii) The medial striate artery (recurrent
artery ofHeubner: a branch of A.C.A.) -»the
inferior half of the anterior limb of the internal capsule. (in)
The internal carotid -> one or more branches to the genu.
71
(iv) The posterior communicating artery -> the anteiror 1/3 of the ventral half of the
posterior limb of the internal capsule.
(v) The anterior choroidal artery -» the posterior 2/3 of the ventral half of the posterior
limb of the internal capsule and its retrolenticular part. Venous Drainage of the Brain:
Fine branches -> a pial plexus -> cerebral veins (superficial and deep) -> The sinuses of
the dura mater —»The internal jugular vein. A - Venous Sinuses:
The superior sagittal (longitudinal) sinus : lies along the attached border of the falx
cerebri.
The inferior sagittal (longitudinal) sinus : lies along the free border of the falx. The
sinus rectus (straight sinus) : lies along the line of attachment of the falx and
tentorium. It is formed by the union of:
* the inferior sagittal sinus &
* the great cerebral vein of Galen.
The 2 transverse sinuses:
Each passses laterally and forwards —»internal jugular vein.
The confluence of sinuses: is the point of union of the superior sagittal, straight and
transverse sinuses, together with the unpaired occipital sinus.
The cavernous sinus: is located on the side of the sphenoid bone, lateral to the sella and
consists of a network of vessels enclosing the internal carotid, the 3rd, 4th, 6th and the
ophthalmic division of 5th cranial nerves.
It receives:
* the basilar venous plexus.
* the 2 ophthalmic veins via the orbital fissure.
* the sphenoparietal sinus.
It empties into:
* the superior petrosal sinus -> transverse sinus &
* the inferior petrosal sinus -»jugular vein.
The circular sinus: is a venous ring around the hypophysis formed by: the 2 cavernous
sinuses and their connecting channels. N.B.: The venous sinuses communicate with the
extracranial veins by emissary veins which
perforate the skull. B. The Cerebral Veins:
They are divided into:
1. The Superficial Cerebral Veins: drain the cortex and subcortical medullary substance,
into the superior sagittal sinus and basal sinuses (cavernous, petrosal & transverse).
2. The Deep Cerebral Veins: drain the deep medullary substance, basal ganglia and
dorsal parts of the diencephalon, into the internal & great cerebral veins. The 2 groups
are interconnected by both intracerebral and extracerebral anastomosis. N.,B.: The venous
sinuses & cerebral veins are devoid of valves.
CEREBROVASCULAR ACCIDENTS
Cerebrovascular accidents fall into two groups :
1. Spontaneous intracranial haemorrhage: includes:
(i) Primary intracerebral hemorrhage (20% of cases)
(ii) Subarachnoid hemorrhage (8 % of cases)
2. Cerebral infarction or ischaemia : is caused by :
(i) Cerebral embolism (20% of cases) e.g. in A.F., myocardial infarction & bacterial
endocarditis.
72,
Median surface
Middle
cerebral artery
1. OrbitofrontaJ artery
2. Prerolandic artery
3. Rolandic artery
4. Anterior parietal artery
5. Posterior parietal artery
6. Angular artery
7. Posterior temporal artery
8. Anterior temporal artery
9. Orbital artery
10. Frontopolar artery
11. CallosomarginaJ artery
\2. Posterior internal frontal artery
13. PericaUosal artery-
Scheme of the artenaJ supply of the cerebraJ cortex. (Redrawn and reproduced, with permjssion, from B
Intracranial Tumors. 2nd ed. Thomas. 1948 )
Anterior limb
Posterior limb
Blood Supply of the Internal Capsules:
Anterior cerebral arteries
Anterior communicating artery
Middle cerebral arteries
Circle
of Willis
Internal carotid arteries
Posterior communicating
arteries
Posterior cerebral arteries
Basilar artery
Vertebral arteries
The blood supply to the brain and the cirde of Willis.
(ii) Cerebral thrombosis (50% of cases)
(iii) Cerebral arteriosclerosis and hypertension
(iv) Other causes include:
* Anaemia.
* Hypoxia e.g. cardiac arrest, CO poisoning, & pulmonary emboli.
* Vasospasm e.g. migraine & following subarachnoid hemorrhage
* Micro-emboli (platelets, cholesterol, or fibrin).
* Hypotensive states causing cerebral ischaemia.
* Reversal of cephalic blood flow (subclavian steal syndrome).
* Pregnancy leading to increased coagulability of blood.
* Dehydration leading to haemoconcentration.
* Arteritis e.g. collagen vascular disease.
* Dissecting aortic aneurysm involving the carotid artery.
* Ligation of carotid artery for intracranial aneurysm.
Emmissary veins
Inferior sagittal sinus
Cavernous sinus
Great cerebral vein
Frontal vein
.Rectus sinus Transverse
Ophthalmic
veins
Pterygoid
plexus
Anterior facial vein
Internal jugular vein
sinus Superior petrosal
sinus Inferior petrosal
sinus
Occipital vein Deep
cervical vein
Superior sagittal sinus
The dural venous sinuses
73
CEREBRAL HAEMORRHAGE
Aetiology: It may be arterial, capillary, or venous.
1. Arterial intracerebral haemorrhage is caused by:
(i) Arteriosclerosis: hypertrophy and degeneration of the media with atheroma of
the intima, as well as miliary aneurysms (micro-aneurysms).
(ii) Hypertension: Usually in primary hypertension.
(Hi) Other causes include: developmental vascular anomalies/leukaemia, polyarteritis nodosa and septic embolus in bacterial endocarditis.
2. Capillary orpetechial haemorrhages may occur in:
(i) Acute encephalitis.
(ii) Septicaemia.
(iii) Severe anaemia
(iv) Leukaemia.
(v) Thrombocytopenic purpura.
(vi) Anaphylaxis.
(vii) Haemorrhage into a brain tumour e.g. glioma.
3. Intracranial venous haemorrhage is met with in:
(i) Whooping cough.
(ii) Pyaemia.
Pathology:
* It may affect any part of the brain e.g. the internal capsule, pons, ventricles, or
cerebellum.
* The resultant blood clot may remain encapsulated, or open into one lateral ventricle or
into the subarachnoid space.
* Compression and oedema of the brain tissue surrounding the clot.
* Absorption of the clot with gliosis and phagocytosis of the destroyed brain tissue may
occur.
Clinical Picture:
Age : It is common in late middle age. Sex
: It affects males more than females. Onset:
Sudden, abrupt, or apoplectic. Premonitory
Symptoms include:
(i) Headache
(ii) Vomiting
(iii) Dizziness.
(iv) Vertigo
(v) Syncope.
(vi) Confusion.
(vii) Epistaxis.
(viii) Transient monoparesis and/or dysphasia.
Precipitating Factors: include mental excitement and physical effort
Presenting Symptoms include:
1. Sudden severe headache and vomiting.
2. Loss of consciousness, with or without convulsions.
3. Focal signs depending on the site and size of haemorrhage:
I. Capsular Haemorrhage:
1. Coma.
2. Rotation of the head and deviation of the eyes towards the side of the lesion.
3. Contralateral flaccid hemiplegiaf with flattening of the nasolabial fold, puffing of the
cheek during expiration, hypotpnia, hyporeflexia or areflexia, lost abdominals and
extensor plantar response. Spasticity develops after 2-3 weeks.
4. Contralateral hemianalgesia: Anaesthesia to pin prick.
5. Pulse: Full, bounding, slow pulse.
6. Temperature: Slight pyrexia.
7. Respiration: Deep stertorous respiration or Cheyne-Stokes respiration.
8. B.P.: usually raised.
9. Eyes: * Pupils: unequal.
* Corneal reflex: is lost on the hemiplegic side or bilaterally.
74
* Fundus: Arteriosclerotic retinal vessels with or without slight papilledema.
* Divergent squint may be present
10. Sphincters: Retention or incontinence of urine and faeces. nPontine Haemorrhage: l.Coma.
2. Unilateral pontine haemorrhage results in ipsilateral facial palsy with contralateral
hemiplegia.
3. Bilateral pontine haemorrhage produces quadriplegia with bilateral facial palsy and
bilateral extensor plantar response.
4. Decerebrate rigidity.
5. Pinpoint pupils due to bilateral damage of the ocular sympathetic fibers.
6. Poikilothermia: hyper or hypothermia due to loss of the hypothalamic contol over the
body temperature.
HI- Ventricular Haemorrhage:
1. Deep coma
3. Rigid extension of the upper limbs.
2. Bilateral pyramidal lesion.
4. Hyperpyrexia.
IV- Cerebellar Haemorrhage:
1. Onset is sudden with occipital headache, vomiting and vertigo.
2. Paralysis of conjugate gaze towards the lesion, 6th nerve palsy or skew deviation may
be present.
3. Ataxia: usually trunkal.
4. Coma may occur due to brain - stem compression.
Investigations:
1. CT scan of the brain localizes the hemorrhage
2. Angiography or ventriculography may be indicated to localize the site of the clot
3. C.S.F.: Lumbar puncture carries the risk of tentorial or cerebellar herniation so it is
only done if necessary for diagnosis. CSF shows increased proteins, raised pressure ±
blood or RBCs.
4. Heart is enlarged from chronic hypertension.
5. Urine; albuminuria and glycosuria.
Differential Diagnosis:
Intracerebral haemorrhage has to be distinguished from:
1. Cerebral thrombosis or atheroma.
2. Cerebral embolism.
3. Primary subarachnoid haemorrhage.
4. Intracranial tumour.
5. GPI and meningovascular syphilis.
Prognosis:
* Death occurs in most cases within few hours to few days.
* Causes of death include: medullary anaemia, increased ICT, destruction of brain
tissue, and intercurrent infection e.g. pneumonia which may occur during coma.
* Bad prognosis is expected in:
(i) Bilateral paralysis of limbs.
(ii) Bloody C S F.
(iii) Deep coma continuing more than 48 hours.
* Few patients recover from coma with permanent disability e.g. impaired intelligence,
speech and memory, irritability, emotional instability, hemiplegia, hemianaesthesia,
hemianopia, thalamic pain, and/or extrapyramidal involuntary movements such as
chorea, athetosis or Parkinsonian tremors.
Treatment:
(A) Conservative:
1. The patient should be moved as little as possible.
2. Nursing care.
3. Steroids to reduce cerebral oedema.
75
4. Avoid hypotensive drugs, as they may aggravate the condition.
(B) Surgical evacuation of the clot is indicated in young patients after localization by CT
scanning, angiography or ventriculography.
SUBARACHNOID HAEMORRHAGE (S.A.H.)
Aetiology:
1. Ruptured intracranial aneurysm is the commonest cause. (85%)
2. Ruptured intracranial angiomatous malformations. (10%)
3. Other causes include:
(i) Head injury.
(ii) Acute encephalitis or encephalopathy with capillary damage and haemorrhage.
(iii) Haemorrhagic diseases.
(iv) As a complication of anticoagulant therapy.
(v) Intracranial tumours e.g. angioblastic meningioma, glioma, metastatic melanoma
and other metastases. (vi) Cheese syndrome (acute hypertensive reaction) : in
patients ingesting cheese
while receiving one of the amine-oxidase inhibitor drugs,
(vii) Cerebral atheromatosis with hypertension, (viii) Angioma
of the spinal cord.
Clinical Picture :
1. Age : 2nd and 3rd decades in angioma, 4th and 5th decades in aneurysm.
2. Sex : both sexes, but females more than males.
3. Increased ICT:
(i) Severe headache.
(ii) Vomiting.
(iii) Slight papilloedema.
(iv) Convulsions.
(v) Deep coma with irregular breathing and slow pulse may occur or the patient
may be only confused.
(vi) Retinal haemorrhages, subhyaloid or vitreous haemorrhages may occur, (vii)
Hyporeflexia or areflexia, lost abdominals and extensor plantar responses, (viii)
Hyperpyrexia, transient arterial hypertension, albuminuria and glycosuria may
occur due to hypothalamic damage.
4. Meningeal Irritation (Meningism):
(i) Neck rigidity.
(ii) Positive Kernig's sign.
(iii) Opisthotonos may occur.
(iv) Low backache and pain in the back of the neck.
5. Focal Symptoms : (due to compression by a blood clot, cerebral haemorrhage, or in
farction).
(i) Visual field defect.
(ii) III, IV & VI cranial nerve palsies,
(iii) Frontal lobe haemorrhage produces mental symptoms, hemiparesis, and motor
aphasia in left-sided lesions.
(iv) Convulsions and monoplegia (middle-cerebral), (v) Crossed homonymous
hemianopia (posterior cerebral), (vi) Quadriplegia or crossed hemiplegia (basilar
artery), (vii) Spinal subarachnoid haemorrhage; gives low back pain and pain in lower
limbs,
sphincteric disturbances, stiffness of the spine, Kernig's sign, flaccid weakness
of the L.Ls. with anaesthesia and areflexia.
6. Cranial signs: e.g. cranial bruit, angioma of the face and pulsating exophthalmos.
76
Differential Diagnosis of Cerebrovascular Disorders
Features
Intracerebral
Heamorrhage
Cerebral
Thrombosis
Cerebral
Embolism
Subarachnoid
Haemorrhage
Age
Common between 40 &
50 years
Common over 50
years
Any age, but common
below 40
2 nd & 3rd decades in
angioma 4th & 5 th
decades in aneurysm.
Onset
Dramatic & apoplectic.
Rapid, over minutes to
Generally during activity. hours. Unrelated to
activity
Sudden within seconds
or minutes. May be
ushered by
convulsions. Unrelated to activity
Sudden onset of severe
headache. Unrelated
to activity.
Prodromal Severe headache, vomitsymptoms ing, epistaxis & syncopy
may accur
Course
Dizziness, aphasia, hemi- Usually no prodrome
paresis & hemiparaesthesias, with improvement between attacks.
Rapid hemiplegia & other Rapid improvement at
phenomena e.g. convulse times
ions over minutes to one
hour
Conscious- Rapid progression to
ness
deepening coma.
Relatively preserved
Recurrent stiff neck,
headaches, Low back
pain, ophthalmoplegia,
convulsions & syncope
Rapid improvement
may accur
Variable,worst in initial
few days after onset
Relatively preserved
Relatively brief disturbance of consciousness.
Differential Diagnosis (Cent.)
Investigations:
1. CT Scan of the Brain discloses the S.A.H. in most cases.
2. Lumbar Puncture & CSF Examination are helpful provided no papilledema or lateralizing neurologic signs.CSF shows the following:
(i) Red cells are present in the first week.
(ii) Xanthochromia (yellow coloration of the supernatant fluid) for 2-3 weeks,
(iii) Raised protein content.
(iv) Mononuclear pleocytosis.
(v) Paretic colloidal gold curve may be present.
3. Plain X - ray skull : may show calcified angioma, calcification in the wall of an
aneurysm, abnormal vascularity, and erosion of bone.
4. Angiography: should be done except in very old people, severe shock, severe
atheroma, or hypertension which make surgery impossible. Bilateral carotid
angiography should be done, as multiple aneurysms may be present. Angiography is
negative in about 25% of cases.
Prognosis:
(i) 40 to 50% of patients die within 8 weeks.Two thirds of them die within 24 hours
from the first attack.The remaining one-third die from a second more serious attack
usually in the second week after the first attack, (ii) 10% of the surviving
patients die within 6 months, and another 10% die
subsequently due to recurrent bleeding, (iii) Out of the long-term survivers (30%):
10% are symptom-free, 10% are disabled by
hemiplegia, epilepsy, headache or psychoneurosis, and the remainder (10%) have
minimal residual symptoms.
Treatment:
(A) Medical Treatment: is indicated in the acute phase, in multiple aneurysms or huge
angioma and when aneurysm is surgically inaccessible.
1. Complete bed rest for 4 weeks at least.
2.Sedation and relief of headache e.g. by pethidine or morphine.
3. Prophylactic antibiotics to guard against respiratory and urinary infection.
4.Avoid straining and physical exertion
5. Dehydrating measures, e.g. Mannitol 20%, 1 gm/ kg wL i.v. over 15-20 min. &
Dexamethasone, 4 - 8 mg i.v. 6 hourly.
6.Lumbar puncture.
7. Open bowels.
8. Treatment of coma as usual.
(B) Surgical Treatment: The optimal time for operation is one week after the
haemorrhage.
1. Carotid ligation is beneficial in posterior communicating artery aneurysms, but it
may be complicated by hemiplegia.
2. Direct attack on middle cerebral artery aneurysms e.g. by excision of the aneurysmal
sac or application of a surgical clip to its neck.
CEREBRAL EMBOLISM
Aetiology: Refer to vascular causes of hemiplegia
CEREBRAL THROMBOSIS
Aetiology: Refer to vascular causes of hemiplegia
Management of Cerebral Ischaemia: (Cerebral Thrombosis and Embolism)
(A) General Management includes:
1. Changing the position of the patient in bed every two hours.
2. Care of the skin: using alcohol and talc powder to guard against bed- sores.
77
3. Care of the bladder e.g. catheterization in cases of retention of urine.
4. Care of Respiration:
(i) Suction of secretions
(ii) Bronchoscopy.
(iii) Tracheotomy is sometimes necessary.
5. Treatment of heart failure if present e.g. by digitalis and diuretics.
6. The patient's nutrition and electrolyte balance:
Tube feeding or i.v. fluid therapy may be needed.
7. Paraldehyde 15-30ml. may be given in case of insomnia
(B) Physiotherapy:
1. Keep the patient's limbs in the optimal position using sandbags.
2. Massage to improve the circulation in the paralysed muscles.
3. Short-wave or infra-red therapy.
4. Passive movements.
5. Active exercises.
6. Mobilization and rehabilitation.
(C) Specific Therapy:
1. Anticoagulants: are most helpful for transient cerebral ischaemia (Transient is chaemic attacks). Completed stroke could not be helped by anticoagulant therapy.
Indications.
(i) Carotid T.I.As. (transient ischemic attacks)
(ii) Vertebral-basilar T.I.As.
(iii) Cerebral embolism,
(iv) Deep thrombophlebitis with or without pulmonary embolism.
Contra-indications:
(i) Elderly patients (over 60).
(ii) Severe hypertension.
(iii) Blood diseases,
(iv) Drugs potentiating oral anticoagulants e.g. salicylates, aspirin, butazolidin, dilantin,
sulfisoxazole, tetracyclines, chloramphenicol, neomycin, quinidine, and chloral
hydrate.
(v) Uraemia, liver failure and shock.
Anticoagulants include:
(a) Heparin:
S.C. : 7000 - 9000 U., 6-hourly.
orl.V.: 5000-8000 U.,4-hourly.
OR
10,000 U. every 6 hours, or I.V.
infusion at a rate of 1000 - 1500 U /hr.
* Lee-White clotting time or activated clotting time should be determined before initiating therapy (Normally 6-15 minutes ) and once every 24 hours. A good therapeutic
effect is achieved when C.T. becomes 1.5-2 times the pretreatment value.
* The Antidote for heparin is protamine sulfate 1% which is given in physiologic saline
I.V. (1 mg. for each 100 U. heparin).
(b) Oral Anticoagulants:
Preparations
Dosage
1st. day
(i) Dicumarol 200 - 400 mg. 30
(ii) Warfarin
- 50 mg. 200
(iii) Dindevan
mg.
2nd. day
Daily maintenance
100- 200 mg.
10- 15 mg.
100
mg.
100 mg.
7.5 mg. 50
mg.
* A good therapeutic effect is achieved when the prothrombin time is 2 - 2.5 times the
control.
78
* Barbiturates, doriden, meprobamate and griseofulvin reduce the anticoagulant effect
of these drugs.
* The Antidote for oral anticoagulants: is Vitamin K slowly I.V. + Transfusions of fresh
citrated blood.
* Usually we start with heparin and dindevan together for 48 - 72 hours, after which
heparin is withdrawn and the patient is kept on a maintenance dose of dindevan,
judged by prothrombin time values.
* Many neurologists prefer to use heparin alone for 1 - 2 weeks, shifting to oral
anticoagulants after 2-3 days of overlapping therapy.
2. Antiplatelet Therapy e.g. by Acetylsalicylic Acid (Aspirin ) &/ or Dipyridamole
(Persantin ) may be used in TIAs after, a short course of conventional
anticoagulation.
3. Vasodilators: e.g. papaverine HC1, nicotinic acid, hydergine, ... etc. are frequently
prescribed but their value is doubtful. Moreover, they may cause "internal steal" due
to dilatation of the relatively healthy cerebral vessels, diverting the blood away from
the ischaemic area.
4. Correction of B.P. changes e.g. by hypotensive drugs in hypertension and by
vasopressors in hypotension.
5. Other drugs : e.g.
(i) Lipolytic agents e.g. clofibrate for atherosclerosis,
(ii) Muscle relaxants for spasticity. (iii) Corticosteroids
for cerebral oedema, (iv) Chlorpromazine for
excitement, (v) Antidepressants for depression.
6. Treatment of the cause in cerebral embolism: e.g. A.F., or bacterial endocarditis.
7. Surgery:
* It is hazardous in acute strokes as haemorrhage in the infarcted area is liable to
occur.
* It is also of no value in complete occlusion of the carotid or vertebral arteries.
* Surgical correction is indicated in stenosis of the proximal carotid artery or of the
vertebral artery that narrow the lumen more than 50% as shown by angiography.
Thromboendarterectomy and a bypass graft are the well-known operative measures.
HYPERTENSIVE ENCEPHALOPATHY
Definition: An acute transient disturbance of cerebral function due to arterial hyperten sion of any cause, manifested clinically by convulsions and focal symptoms e.g. hemiplegia, aphasia, or blindness.
Aetiology:
Arterial hypertension e.g. in acute and chronic glomerulonephritis, eclampsia and
malignant hypertension. This results in vasoconstriction of the cerebral arterioles, which
causes the characteristic symptoms.
Clinical Picture:
1. Onset: is subacute
2. Progressive headache.
3. Vomiting.
4. Convulsions.
5. Mental confusion or coma.
6. Aphasia.
7. Hemiparesis.
8. Blurring of vision or blindness.
9. Arterial hypertension.
10. Puffness of the face.
11. Bilateral papilloedema with or without hypertensive retinopathy may be present.
12. Neck rigidity, tachycardia and fever may be present.
13. EEC: shows diffuse slow activity with loss of the alpha rhythm and absence of the
"following" response to photic stimulation.
79
14. CSF pressure: is increased. Differential
Diagnosis: It must be distinguished from:
1. Uraemia
2. Brain tumour.
3. Meningitis.
4. Cerebrovascular strokes e.g. haemorrhage or thrombosis. Prognosis : is on the
whole good and recovery is the rule, but severe and frequent
convulsions are a bad sign.
Treatment:
1. Hypotensive drugs e.g. Nifedipine (Adalat) sublingual or sodium nitroprus side(Nipride) i.v. infusion.
2. Dehydrating measures for brain oedema e.g. Dexamethasone (Decadron) i.v. & / or
diuretics as i.v. frusemide (Lasix) or Mannitol 20% 1 gm/kg. body wt. i.v. over 15 20 min.
3. Barbiturates or paraldehyde i.m. for convulsions.
4. Treatment of the cause e.g. treatment of nephritis.
SYNDROMES OF THE CEREBRAL ARTERIES
INTERNAL CAROTID ARTERY OCCLUSIVE SYNDROMES:
(A) Carotid Insufficiency : results in recurrent transitory attacks of:
1. Unilateral frontal headache.
2. Transient blindness in the ipsilateral eye.
3. Contralateral paraesthesiae or hemiparesis.
4. Convulsions
5. Confusion.
6. Aphasia or dysphasia.
(B) Carotid Occlusion:
1. Ipsilateral blindness or blurring of vision (Ophthalmic artery occlusion)
2. Contralateral hemiplegia.
3. Contralateral hemi-anaesthesia (usually cortical).
4. Crossed homonymous hemianopia (temporal hemianopia in the opposite visual field).
5. Aphasia (sensory & motor) in left-sided lesions.
6. Carotid pulse may be diminished or lost and audible bruit may be present over a
stenotic carotid artery.
7. Carotid angiography is diagnostic.
N.B.: Coma may occur at the onset.
MIDDLE CEREBRAL ARTERY OCCLUSIVE SYNDROMES :
(A) Main Artery Occlusion :
1.
2.
3.
4.
Coma at the onset.
Contralateral hemiplegia most marked in the face, tongue & U.L.
Contralateral hemianesthesia (cortical sensory loss).
Crossed homonymous hemianopia (due to infarction of the optic pathways in the
temporal lobe).
5. Global aphasia in left-sided lesion (dominant hemisphere).
(B) Ganglionic Branches Occlusion (Lenticulooptic & Lenticulostriate): produces
Capsular hemiplegia:
1.
2.
3.
4.
80
Complete hemiplegia on the opposite side.
Hemianaesthesia (usually subcortical in type).
Hemianopia may be present.
Usually no coma, convulsions or aphasia.
(C) Cortical Branches Occlusion :
1. Frontal branch occlusion :
(i) Facio-ftrachial monoplegia.
(ii) Motor aphasia in left-sided lesion.
2. Parietal branches occlusion :
(i) Hemianesthesia.
(ii) Receptive aphasia (Visual agnosia) and apraxia in left-sided lesions.
3. Temporal branches occlusion :
(i) Receptive aphasia (Auditory agnosia) in left-sided lesion, (ii)
Crossed homonymous hemianopia.
ANTERIOR CEREBRAL ARTERY OCCLUSIVE SYNDROMES :
(A) Main Trunk Occlusion :
1. Contralateral hemiplegia, L.L. is more affected than U.L. (due to infarction of the
leg area in the motor cortex).
2. Contralateral cortical anesthesia in the L.L. (due to infarction of the leg area in the
sensory cortex).
3. Mental confusion, in left-sided lesion.
4. Motor aphasia, in left-sided lesion.
5. Clouding of consciousness, in left-sided lesion.
6. Apraxia on the left side.
7. Forced grasping & groping reflexes on the paralysed side.
(B) Heubner's Artery Occlusion :
1. Contralateral facio-brachial monoplegia, proximal more than distal, with sensory loss
of the spinothalamic type.
2. Mental deterioration in left-sided lesion.
3. Motor aphasia in left-sided lesion (due to infarction of the subcortical white matter
beneath Broca's area).
(C) Paracentral Artery Occlusion :
1. Contralateral spastic monoplegia (L.L.) with or without cortical sensory loss (due to
infarction of the leg area on the paracentral lobule).
2. Urinary incontinence.
(D)Occlusion of Both Anterior Cerebral Arteries : e.g. by anterior communicating artery
aneurysm
1. Dementia & apathy.
2. Long tract signs.
3. Bilaeral grasp reflexes may be present.
ANTERIOR CHOROIDAL ARTERY OCCLUSIVE SYNDROME :
1. Hemiplegia.
2. Hemianesthesia.
3. Hemianopia.
N.B.: This syndrome must be differentiated from middle cerebral artery ocelusive syn drome by the absence of coma & the better prognosis.
POSTERIOR CEREBRAL ARTERY OCCLUSIVE SYNDROMES :
(A) Main Trunk Occlusion :
1. Contralateral homonymous hemianopia with escape of the macular region.
2. Visual agnosia in left-sided lesion.
3. Thalamic syndrome.
4. Temporal lobe seizures may occur.
(B) Thalamo-geniculate artery occlusion (Thalamic syndrome):
1. Temporary flaccid hemiparesis or hemiplegia.
2. Impairment of superficial & loss of deep sensation.
81
3. Thalamic pain or thalamic hyperpathia (spontaneous, agonizing burning pain).
4. Reflex dystrophy of the shoulder girdle & arm.
5. Choreo-athetoid movements, ataxia or tremor.
All these manifestations occur on the opposite side of the lesion.
(C) Thalamoperforationg artery thrombosis : results in choreo-athetoid movements of
the opposite arm & leg (due to infarction of the termination of the
dentato-rubro-thalamic pathway & subthalamic structures).
(D) Cortical Branches Occlusion :
1. Occipital branches occlusion (Calcarine branches thrombosis) : Contralateral ho monymous hemianopia with macular sparing.
2. Parietal branches occlusion : Visual agnosia in left-sided lesion.
VERTEBROBASILAR ARTERY OCCLUSIVE SYNDROMES :
(A) Vertebrobasilar Insufficiency:
1. Syncope or drop attacks (transient loss of postural tone).
2. Ophthalmoplegia & diplopia.
3. Vertigo, nausea, vomiting & deafness (internal auditory artery occlusion).
4. Ataxia.
5. Nystagmus.
6. Bilateral pyramidal signs with bulbar palsy.
7. Bilateral dysesthesiae.
8. Migraine-like attacks or visual hallucinations may occur.
(B) Basilar Artery Occlusion :
1. Deep coma.
2. Small pupil fixed to light
3. Unilateral or bilateral 3rd , 4th & 6th nerve palsies.
4. Pseudobulbar palsy &quadriplegia with decerebrate rigidity.
5. Rapidly fatal (death usually occurs in 2 to 5 days).
(C) Paramedian Branches Occlusion (Crossed hemiplegias):
1. In the midbrain :
(i) Weber's syndrome : (infarction of tthe oculomotor nucleus & cerebral peduncle).
* Ipsilateral 3rd nerve palsy (ophthalmoplegia).
* Contralateral hemiplegia.
(ii) Benedikt's syndrome : (infarction of the oculomotor nucleus, cerebral peduncle,
medial lemniscus & red nucleus)
* Ipsilateral ophthalmoplegia.
* Contralateral hemiplegia, hemianesthesia, & choreiform movements.
2. In the pons :
(i) Millard-Gubler's syndrome :
* Ipsilateral 6th & 7th nerve palsies.
* Contralateral hemiplegia.
(ii) Foville's syndrome:
* Ipsilateral L.M.N facial palsy.
* Paralysis of the conjugate gaze to the side of the lesion.
* Contralateral hemiplegia.
3. In the medulla oblongata :
(Infarction of the 12th nerve nucleus, the pyramid & the medial lemniscus).
* Paralysis & atrophy of the homolateral half of the tongue.
* Contralateral hemiplegia & hemianesthesia.
(D) Cortical Branches Occlusion:
1. Posterior cerebral occlusive syndromes: were discussed before.
2. Cerebellar Arteries Occlusion:
(i) Superior Cerebellar Artery Occlusive Syndrome:
82
(a) Ipsilateral:
* Choreiform movements (due to damage to the brachium conjunctivum).
* Homer's syndrome.
* Deafness may occur.
* Facial palsy may occur.
(b) Contralateral: analgesia & thermo-anesthesia (due to damage of the
trigeminothalamic & spinothalamic tracts).
(ii) Anterior Inferior Cerebellar Artery Occlusion:
(a) Ipsilateral:
* Cerebellar ataxia.
* Horner's syndrome (due to damage of the descending sympathetic fibres).
* Deafness (8th).
* Facial palsy (7th).
* Loss of touch sensibility in the face (main sensory nucleus of 5th nerve nerve).
(b) Contralateral: analgesia & thermo-anesthesia.
(iii) Posterior Inferior Cerebellar Artery Occlusion:
(Wallenberg's syndrome or Lateral Medullary syndrome)
(a) Onset: with severe vertigo, hiccup, vomiting, dysphagia & pain or paraesthesiae over the face.
(b) Ipsilateral:
* Cerebellar ataxia.
* Nystagmus (due to damage of the vestibular nuclei).
* Horner's syndrome.
* Dissociated sensory loss over the face (due to damage of the spinal tract &
nucleus of the 5th nerve).
* Dysarthria & dysphagia due to weakness of the homolateral palatal muscles
(damage of the nucleus ambiguus of the vagus).
(c) Contralateral : analgesia & thermo-anesthesia (due to damage of the spinal
lemniscus).
3. Spinal Artery Occlusion : (i) Thrombosis of the anterior spinal artery may
occur due to atherosclerosis &
produces massive infarction of the spinal cord with a complete flaccid paraplegia,
retention of urine and sensory loss to pain and temperature below the level of the
lesion with preservation of touch and proprioceptive sensations (posterior
column). Complete quadriplegia with respiratory paralysis and death occur in
upper cervical lesions, (ii) Embolism or occlusion of radicals of the anterior
spinal artery produces
incomplete infarction with paraparesis. (iii) Intermittent claudication (ischaemia)
of the spinal cord or of the cauda equina
may follow exertion and relieved by rest.
Radiography and myelography may show bony stenosis of the spinal canal or a
central disc protrusion in these cases.
Laminectomy and decompression improve the condition.
83
CHAPTER 5
HYDROCEPHALUS
ANATOMY : THE VENTRICLES AND CSF CIRCULATION
There are 4 ventricles in the brain - 2 lateral ventricles,
- the third ventricle &
- the fourth ventricle.
The 2 lateral ventricles are the cavities of the two cerebral hemispheres.
Each consists of: a body , anterior horn (frontal), posterior horn (occipital) and inferior
horn (temporal).
* The lateral ventricle communicates with the 3rd ventricle through the foramen of
Monro (interventricular foramen).
* The choroid plexus of the lateral ventricle : is a vascular process of pia mater
projecting into the ventricular cavity . It receives its blood from 2 arteries:
(i) the anterior choroidal artery (from internal carotid artery) (ii) the posterior choroidal
artery (from posterior cerebral artery) The Third ventricle is a narrow vertical cleft
between the two lateral ventricles, bounded on both sides by the 2 thalami.
* It communicates with the 2 lateral ventricles through the foramina of Monro and with
the fourth ventricle through the cerebral aquenduct. (aqueduct of Sylvius).
The Fourth ventricle: is the cavity of the brain-stem, bounded ventrally by the pons
and medulla, dorsally by the cerebellum, and laterally by the superior, middle &
inferior cerebellar peduncles, the cuneate tubercles and the claves.
* It is a continuation of the cerebral aqueduct to the central canal of the medulla.
* It communicates with the 3rd ventricle through the aqueduct of Sylvius and with the
subarachnoid space through the foramina of Luschka and Magendie (lateral and
medial apertures).
N.B.: The normal ventricular capacity ranges from 7 to 30 cc.
CSF Formation:
* CSF is mostly formed by the choroid plexuses of the ventricles particularly that of the
lateral ventricles (95%).
* Diffusion through ependymal and pial vessels is a probable source of the CSF.
CSF Circulation:
The CSF formed in the lateral ventricles —> Foramina of Monro —> 3rd ventricle —»
aqueduct of Sylvius -> 4th ventricle —> foramina of Luschka and Magendie —>
subarachnoid spaces, diffuses over the brain and spinal cord —> arachnoid villi —» venous
sinuses —> Jugular veins. CSF Absorption :
CSF is absorbed by the arachnoid villi to the dural venous sinuses and also by the pial
veins. Function of
CSF:
(i) Protection of the brain and spinal cord by absorbing the shock.
(ii) Convey nutritive materials to the CNS.
(iii) Excretion of metabolites.
(iv) Compensation for changes in intracranial volume.
84
N.B.: Queckenstedt's test: Compressing the jugular veins during lumbar puncture ->
prompt rise in CSF pressure with prompt return to normal level on release of
compression.
* Complete or partial spinal block -> absence of pressure rise or a slow rise and a slow fall
on compression of both jugular veins.
* Thrombosis of the lateral sinus —> absence of pressure rise on compression of the ipsilateral jugular vein.
N.B.: Froin's Syndrome : Xanthochromia ± cyto-albundnous dissociation + subarachnoid
DiOCK.
Superior sagittal sinus
Arachnoid villi
. The normal direction of cerebrospinal fluid flow (indicated by the arrows) as seen schematically
from an anterior view.
Dura mater
Arachnoid mater
Sutaarachnoid space
Pia mater (adherent to
the brain and spinal
cord)
Lateral ventricle
•Third ventricle
Cerebral aquaduct
Fourth ventricle
Foramen of Luschka
Foramen of Luschka
Foramen of Magendie
flow (indicatec
HYDROCEPHALUS
Definition : increased volume of C S F within the skull.
Varieties:
1. Compensatory hydrocephalus: increased volume of CSF with normal pressure.
2. Hypertensive hydrocephalus: both CSF volume and pressure are increased.
It includes:
(a) Obstructive hydrocephalus (non-communicating): due to obstructed CSF circulation.
(a) Communicating hydrocephalus : due to increased formation and impaired absorption
of CSF, or obstruction in the subarachnoid space e.g. by adhesions of meninges fol
lowing meningitis.
Causes:
1. Compensatory hydrocephalus: may occur in :
(i) Cogenital cerebral hypoplasia.
(ii) Acquired cerebral atrophy : e.g. M.S., G.P.I., senile or presenile dementias, in
some epileptics and post-traumatic after severe head injury.
2. Hypertensive hydrocephalus:
(a) Obstructive hydrocephalus: is due to obstruction of the CSF flow from the ventricles to the subarachnoid space e.g. i. Obstruction within the third ventricle e.g. by
a neoplasm.
85
ii. Obstruction of the cerebral aqueduct (aqueduct of Sylvius) e.g.
* Congenital aqueduct stenosis or atresia.
* Gliosis or obstruction by tumours of the 3rd ventricle, midbrain or pineal
body.
iii. Obstruction of the fourth ventricle or its foramina by a posterior fossa tumour,
or by adhesions following meningitis, (b)
Communicating hydrocephalus : is due to: i.
Increased CSF formation : e.g. in :
* Meningism : lowering the osmotic tension of the blood.
* Papiloma of the choroid plexus.
* Meningitis causing congestion of the choroid plexus.
* Vitamin A deficiency and hypervitaminosis A.
ii. Obstruction of the cranial subarachnoid space : e.g. by a tumour,adhesions
following meningitis, trauma or subarachnoid haemorrhage, or congenital,
anomalies such as the Arnold-Chiary malformation or basilar impression.
iii. Impaired absorption of the CSF due to :
* Compression of venous sinuses by a brain tumour.
* Raised intrathoracic pressure impeding venous return.
* Superior sagittal sinus thrombosis secondary to lateral sinus thrombosis
complicating otitis media or mastoiditis (Otitic hydrocephalus).
* Meningitis causing obliteration of the arachnoid villi.
Pathology:
(i) Distension of the ventricles.
(ii) Thinning of the cerebral hemispheres.
(iii) Meningeal adhesions in post-meningitic cases.
(iv) Thinning of the skull bones, separation of the sutures in young patients, erosion of
the chinoid processes and excavation of the sella turcica (v)
Atrophy of the optic nerves and olfactory tract is frequent.
Clinical Picture:
(A) Infantile Hydrocephalus:
1 . Enlarged head, with separated sutures, enlarged anterior fontanelle, and congested
veins.
2 . A fluid thrill on percussion and an audible murmur on auscultation may be found.
3 * Forward and downward protrusion of eyes (rising sun sign)
4 . Absent or slight symptoms of increaed ICT. e.g. headache,vomiting & papilloedema.
5 . Convulsions, optic atrophy, and bilateral anosmia are common.
6 . Progressive deterioration of visual acuity up to blindness.
7 . Other cranial nerve palsies may occur. Squint and nystagmus may be present.
8. Weakness, spasticity, hyperreflexia, extensor plantar responses and incoordination are
common in the lower limbs than in the U.Ls. 9
. Mental deficiency in severe cases.
10. Obesity in mild cases due to hypothalamo-hypophyseal compression.
Wasting occurs in severe cases.
11. Cerebrospinal rhinorrhoea is rare.
(B) Hydrocephalus after Infancy :
Obstructive hydrocephalus:
1. Symptoms of increased ICT are marked e.g. headache, vomiting and papilloedema.
2. Head retraction, opisthotonos and impaired consciousness may occur.
3. Giddiness is common.
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4. Mental deterioration, hallucinations, delusions and mood changes.
5. Convulsions are less frequent than in the infantile type.
6. Enlargement of the head is less marked, with slight separation of sutures in cases
starting before the age of 18, leading to a "cracked-pot sound" on percussion.
7. Cranial nerve palsies e.g. 6th & 7th nerve palsies.
8. Slight exophthalmos.
9. Clumsiness and slight incoordination of limbs.
10. Hyperreflexia or hyporeflexia and extensor plantar responses with no sensory loss.
11. Obesity and genital atrophy may occur due to hypopituitarism.
12. CSF pressure is raised in communicating hydrocephalus, but normal or diminished in
the obstructive type.
13. X-ray skull : Enlargement of the cranium, silver-beaten or finger-print appearance,
separated sutures, deepening and expansion of the sella turcica with erosion of the
clinoid processes may be present.
14. Ventriculography: shows marked dilatation of the ventricular system.
Myodil ventriculography and isotope ventriculography may be helpful.
Low pressure hydrocephalus (Hakim-Adams):
1. Age of onset: in middle and late life in most cases.
2. Confusion.
3.Ataxia.
4. Dementia.
5. Air ventriculography shows marked ventricular dilatation, but no subarahnoid air and
the patient deteriorates much after this procedure.
6. Improved by a shunt operation.
Differential Diagnosis:
Infantile hydrocephalus must be distinguished from :
1. Rickets : bony bosses and other signs of rickets.
2. Megalencephaly : by air ventriculography.
Benign Intracranial Hypertension (Toxic hydrocephalus):
Raised CSF pressure in the absence of a space-occupying lesion and without ventricular
enlargement.
(a) Women, in the 4th decade, obese, with pregnancy or miscarriage, with a history of
infection or head injury.
(b) Otitic hydrocephalus is due to transverse or sagittal sinus thrombosis secondary to
otitis media or mastoiditis.
Clinically : Papilloedma, headache, vomiting, diplopia, visual failure and central scotomas.
v
Prognosis:
* Untreated infantile hydrocephalus is fatal in most cases.
* Survivors may show mental subnormality, blindness, or epilepsy.
* In after infancy hydrocephalus, the prognosis depends on the cause.
Treatment:
(A) Infantile hydrocephalus:
1. Drainage of the CSF into the ureter and peritoneal cavity.
2. Drainage of the CSF into the jugular vein by a Spitz-Holter and Pudenz-Heyer
valves.
3. Suboccipital decompression for Arnold-Chiary malformation.
(B) Hydrocephalus after infancy : Treatment is that of the cause e.g.
1. Removal of a brain tumour.
2. Torkilsen's operation of ventriculocisternostomy for aqueduct stenosis.
3. Corticosteroids, diuretics, and repeated lumbar puncture for benign intracranial
hypertension and otitic hydrocephalus.
4. Cranial decompression for visual failure.
87
CHAPTER 6 BRAIN
TUMOURS
CEREBRAL LOCALIZATION
The two cerebral hemispheres are separated by the longitudinal cerebral fissure and connected together at the depth of this fissure by the corpus callosum. The surfaces of
cerbral hemispheres present many fissures (sulci) and convolutions (gyri). Each
cerebral hemisphere is divided into four main lobes: frontal, parietal, occipital and
temporal lobes, as well as two important parts known as insula and rhinencephalon
(limbic system or limbic lobe).
* The lateral cerebral fissure (Sylvian fissure) separates the frontal from the temporal
lobe.
* The central sulcus (Fissure of Rolando) separates the frontal from the parietal lobe.
* The Parieto-occipital fissure separates the parietal from the occipital lobe.
* The precentral sulcus separates the precentral gyrus (area 4 ) from the rest of the fron
tal lobe.
* The superior & inferior frontal sulci divide the rest of the frontal lobe into superior,
middle and inferior frontal gyri.
* The post-central sulcus separates the post-central gyrus (areas 3, 1 & 2) from the rest
of the parietal lobe.
* The intraparietal sulcus divides the rest of the parietal lobe into the superior & inferior
parietal lobules. The supramarginal gyrus is a part of the inferior parietal lobule that
surrounds the upper end of the posterior ramus of the lateral fissure, while the angular
gyrus is that part which surrounds the end of the superior temporal sulcus. The
precuneus is the posterior part of the medial surface of the parietal lobe adjacent to
the parieto-occipital fissure.
* The lateral occipital sulcus divides the lateral surface of the occipital lobe into a
superior and inferior gyrus.
* The calcarine fissure divides the medial surface of the occipital lobe into the cuneus
and the lingual gyrus.
* The superior and middle temporal sulci divide the temporal lobe into superior, middle
and inferior temporal gyri.
* The inferior temporal sulcus separates the inferior temporal gyrus laterally from the
fusiform (occipito-temporal) gyrus medially.
* The transverse temporal gyrus (Heschl's gyrus) occupies the posterior part of the
superior surface of the temporal lobe and is resposible for hearing.
* The parahippocampal gyrus and uncus are responsible for olfaction.
* The island ofReil (insula) occupies the depth of the Sylvian fissure.
* Stimulation of the insula -> epigastric sensations & motor gastric response (belching
or borborygmi).
* The opercula of the insula are portions of the lips of the Sylvian fissure. They include
the orbital, frontal, parietal and temporal opercula.
* Rhinencephalon (Imbic system or visceral brain) includes the portions concerned with
olfaction
The center of each cerebral hemisphere is made of 3 types of myelinated nerves:
1. Commissural (transverse ) fibres: which connect the 2 hemispheres, e,g. the corpus
callosum.
88
* The anterior commissure connects the 2 olfactory bulbs and the 2 piriform areas.
* The hippocampal commissure connects the 2 hippocampi.
2. Projection fibres: include the corticopetal (afferent) and corticofugal (efferent) fibres.
(a) The corticopetal fibres include:
i. the optic radiation (the geniculocalcarine tract).
ii. the auditory radiation.
iii. thalamic radiation.
(b) The corticofugal fibres include:
i. The corticospinal and corticobulbar tracts.
ii. The corticopontine tracts,
iii. Corticothalamic fibres.
iv . Corticorubral tract.
3. Association fibres: join the different parts of the same hemisphere. They include short
and long association finers e.g. the uncinate fasciculus, cingulum, arcuate fasciculus,
superior and inferior longitudinal fasciculi, occipitofrontal fasciculus and fornix.
Brodmann's Classification of the Cortex:
This was very helpful in functional localizations e.g.
Area4 (The primary motor cortex): occupies the precentral gyrus and the anterior wall of
the central sulcus.
* It controls voluntary movements of the opposite half of the body via the corticospinal
and corticobulbar tracts originating from the Betz - cells.
* The body is represented in area 4 inverted upside down.
* Stimulation (irritative lesions) of area 4 —» contralateral jacksonian seizure.
* Destruction of area 4 —» contralateral flaccid hemiparesis or hemiplegia (more marked
distally).
Area 6 (The premotor area) is located anterior to area 4 and constitutes a part of the
extrapyramidal system.
* Stimulation of area 6 -> stereotyped movements with turning of the head and torsion
of the body (if area 4 is ablated beforehand).
* Destruction of area 6 —» forced grasping in monkeys.
* Combined destruction of area 4 & 6 —»contralateral spastic hemiplegia.
Area 8 (frontal eye movement and pupillary change area) is located in the posterior part of
the middle frontal gyrus.
* Stimulation (irritative lesion) of area 8 -> conjugate deviation of the head and eyes to
the opposite side.
* Destruction of area 8 —> paralysis of the conjugate gaze to the opposite side with
deviation of the eyes to the side of the lesion.
Areas 9 ,10 ,11 and 12 (frontal association areas): are responsible for mentality, intelle
ctual functions and emotions. Prefrontal lobotomy (as a treatment of intractable pain,
anxiety, depression, ...etc)-> reduced intellectual functions with decreased vocabulary
functions and emotional changes.
Areas 3 , 1 & 2 (The primary sensory cortex or somesthetic area): occupy the postcentral
gyrus and receive general sensations from the opposite side of the body through the
thalamic radiations.
* Irritative lesions of areas3 , 1 and 2 -» paresthesias of numbness, tingling and electric
shock sensations on the contralateral side of the body (sensory jacksonian seizure)
* Destruction of areas 3 , 1 and 2-> contralateral hemihypoesthesia of the cortical type
(loss of tactile localization and two point discrimination).
N.B. The cortical taste area lies in the area for facial sensations.
Areas 5 & 7 (Sensory association areas): are responsible for stereognosis.
Area 17 ( The primary visual cortex): is located in the occipital lobe.
* Irritative lesions of area 17 —»Unformed visual hallucinations e.g. flashes of light.
* Destructive lesions —»contralateral homonymous hemianopia with macular sparing.
Areas 18 & 19 (Secondary & tertiary visual association areas): area 18 is responsible for
89
visual recognition, area 19 is responsible for visual recall and revisualization of objects.
* Destructive lesions of areas 18 & 19 on the dominant hemisphere produce visual
agnosia.
N.B : (1) Parietal or temporal lobe lesions may cause visual field defects by interruption of
the optic pathways. (2) Temporal lobe lesions may cause visual hallucinations
of formed objects or
subjects.
Area 52 (The primary auditory area) : is located in the Heschl's gyrus (the transverse
temporal gyrus). It receives the auditory radiation from the medial geniculate body which
carries auditory impulses from the cochlea of the ear.
* Irritative lesions of area 52 -> auditory hallucinations e.g. buzzing and roaring.
* Destructive lesions of area 52 -> mild deafness.
Areas 41 & 42 (The cortical secondary & tertiary auditory areas or associative auditory
cortex) surround area 52.
* Destructive lesions of area 41 & 42 in the dominant hemisphere
' -> auditory
agnosia.
Areas 20 , 21, 22 & 38 , (Temporal association areas)
Area 37 : is the language formulation area.
* Destructive lesions of area 37 —> nominal aphasia.
The olfactory area : lies in the uncus and parahippocampal gyrus of the temporal lobe.
* Irritative lesions -»olfactory hallucinations (uncinatefits).
* Destructive lesions —> anosmia.
Area 44 (Broca's area or Motor speech centre ) : is located in the posterior part of the
inferior frontal gyrus of the dominant hemisphere (left hemisphere in rig ht - handed
people).
* Destructive lesions of area 44 —> Motor aphasia.
Area 39 (angular gyrus): is the higher association area of symbol langauge.
* Destructive lesions of area 39 in the left hemisphere —> Sensory aphasia e.g. word
blindness.
Area 40 is the supramarginal gyrus.
Brodmann's areas on the lateral surface of the cerebral hemisphere
8 (FB): Promoter
pyramidal circuit)
Area 4 (FA): Principal Area
motor area area (part of extra- Areas 18-19 (OB-OA): Visual association areas Area 41 (TC):
Primary auditory cortex
The lateral aspect of the cerebrum. The cortical areas are shown according to Brodmann (numbers) and von Econoi
(letters), with functional localizations.
90
Optic nerve
Anterior
Op*ic chiasm
perforated substance
Optic .tract
Infundibulum
Mammillary body
Oculomotor
Trochlear nerve
nerve Crus
Rons
cerebn
Abducens nerve
Trigemmal nerve
Glossopharyngea! nerve
Facial nerve
Hypoglossal nerve
Vestibulocochlear
Pyramidal decussation
nerve Vagus nerve
Spinal accessory
nerve Ventral root C|
Drawing of the anterior aspect of the medulla, pons and midbrain
HI Ventricle
-Stria medullaris
Habenula
Pulvinar
Brochium
Superior colliculus
Lateral geniculate
body
Inferior colliculus
Cerebellor peduncles
Colliculu
Superior
Middle
s
Superior
Inferior
Inferior
Trochlear n
Vestibular area
Medial eminence
Lateral aperture Stria
medullaris (EZ vent)
Facial colliculus
Tuberculu
m
Cuneatus
Post intermediate sulcus
Gracilis
Fasciculu
s
Cuneatus
Gracilis
Post, median sulcus Drawing of the posterior aspect
of the brain stem with the cerebellum removed
BRAIN TUMOURS
Definition : Space-occupying lesions within the skull, whether neoplastic or chronic
inflammatory in origin.
Neoplasms Affecting the Central Nervous System
PATHOLOGLCAL VARIETIES :
1 - Gliomas : 40 - 50 % of all intracranial neoplasms. They include:
1. Medulloblastoma:
(a) Common in children, rare in adults.
(b) Arises in the cerebellum (in the roof of the 4 th ventricle).
(c) Rapidly growing malignant tumour.
(d) Subarachnoid metastases.
(e) Average survival period is 6 to 12 months. (/*) Radiotherapy retards its growth.
2. Glioblastoma (Spongioblastoma) Multiforme:
(a) Middle life.
(b) Arises in the cerebral hemispheres.
(c)Highly vascular with haemorrhage and necrosis.
(d) Extremely malignant
(e)Average survival period is 12 months after operation.
3. Astrocytoma:
(0)Any age.
(b) Arises in the
cerebral, or in the cerebellar hemispheres.
(d) Cystic transformation is frequent.
(c) Slowly growing and relatively benign.
4. Oligodendroglioma: Rare
(6)Arises in the cerebral hemispheres.
(a)Young adults.
(e) Calcification may occur.
(c)Slowly growing and relatively benign.
(d) Malignant anaplasia may occur.
5. Ependymoma : Rare
(a) Arises in the roof of the 4 th ventricle, walls of other
ventricles, or from the central canal of the spinal cord.
(6)Rosette formation.
6. Ganglioglioma, Ganglioneuromas, and Neuroblastomas are rare.
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II - Meningiomas : 10%
(a) Attached to the dura, but arising from the arachnoid cells of the arachnoid villi.
(b) The cells are arranged in columns or whorls.
(c) Meningioma may contain small calcified concretions (psammoma bodies).
(d) Meningioma is usually single, large and lobulated tumour but rarely it may form a
flat plaque.
(e) It invades the overlying bone in 20 % of cases, with bone absorption and new bone
formation (hyperostosis).
(f) It does not invade the brain bur compresses it.
(g)Meningiomas are usually found along the venous sinuses, e.g. parasagittal
meningiomas, meningiomas of the convexities, sphenoidal ridge meningioma,
olfactory groove meningiomas, suprasellar meningiomas, tentorial meningioma and
intraventricular meningiomas.
(h) Multiple meningiomas are occasionally seen with multiple neurofibromatosis. (i)
Meningiomas are common is females than in males and are rare before middle life. (/)
X - ray base of the skull may show enlargement of the formen spinosum, which
transmits the middle meningeal artery.
HI - Acoustic Neuroma : 5 - 10 %
(a) Usually unilateral, rarely bilateral as a part of multiple neurofibromatosis (von
Recklinghausens disase).
(b) The commonest site of neuroma is the 8 th nerve, but may occur upon the optic,
trigeminal, the dorsal roots of spinal nerves and upon peripheral nerves.
(c) It consists of elongated cells like spindle fibroblasts, with palisading and parallelism
of nuclei.
IV - Tumours of the Blood Vessels:
1. Angiomatous Malformations : are congential abnormalities of vascular development.
Two types:
(a) Telangiectases or capillary angiomas : consist of dilated capillaries.
(b) Arteriovenous Malformations: consist of dilated tortuous cortical vessels usually in
the field of the middle cerebral artery. Clinically: increased vascularity of the scalp,
pulsating arteries, hypertrophy of carotids, bruits over one or both carotids and over
the angioma.
2. Cavernous Haemangiomas : are congenital abnormalities, usually supra - tentorial,
forming a lobulated mass of blood - filled spaces.
3. Haemangioblastomas:
(a) They are vascular channels and spaces with a tendency to form cysts containing
xanthochromic fluid.
(b) The tumour may appear as a small nodule in the wall of a large cyst.
(c) Usually subtentorial (cerebellar ) and single, rarely multiple tumours occur in the
cerebellum with or without a tumour in the medulla or spinal cord.
(d) A cerebellar haemangioblastoma may be associated with a haemangioblastoma of
the retina (Von Hippel's disease).
(e) It may be associated with a haemangioblastoma of the spinal cord, polycystic
pancreas and kidneys , hypernephromas of the kidneys or the suprarenal glands
(Lindaus disease).
(f) Polycythaemia.
(g) Positive family history in 20 % of cases.
4. Sturge - Weber Syndrome:
(a) A capillary - venous malformation, commonly in the parieto - occipital region, with a
11
wavy " pattern of subcortical calcification that outlines the gyri.
(b) A " port - wine" stain on the affected side of the face. (c) Buphthalmos (ox eye ).
(d) A contralateral hemiparesis and epilepsy.
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V - Craniopharyngiomas : (tumours of the craniopharyngeal or Rathke's pouch, adamantinomas, or hypophysial epidermoids)
(a) Usually suprasellar, occasionally intrasellar.
(b) Cystic degeneration, calcification and bony changes are frequent.
VI- Pituitary Tumours : 5%
1. Chromophobe adenoma: is the commonest and produces " hypopitidtarism"'.
2. Acidophil adenoma: produces " hyperpituitarism" i.e. acromegaly in adults and
gigantism if occurs before puberty.
3. Basophil adenoma : is of microscopic size and produces Gushing's syndrome.
4Adenocarcinoma of the pituitary is rare.
5. Intrasellar metastases are rare e.g. from cancer breast.
VII - Cholesteatoma (Cerebrospinal epidermoid):
(a) Rare; affects adults, males more than females.
(b) Sites; in the subarachnoid cisterns at the base of the brain e.g. in the cerebellopontine
angle, ventral aspect of the cerebellum, 4 th ventricle, or in the temporal bone.
VIII- Tumours of the Pineal Gland (Pinealomas): are rare. They were considered
atypical teratomas.
IX - Colloid Cysts of the Third Ventricle : arise from the choroid plexus and cause
hydrocephalus.
X - Papilloma of the choroid plexus : is commoner in the 4 th ventricle than in the lateral
or 3 rd ventricles. It may cause recurrent subarachnoid haemorrhage or communicating
hydrocephalus.
XI - Glomus Jugulare Tumours: may invade the middle ear or the posterior fossa.
Clinically : (a) Unilateral deafness . (b) Multiple cranial nerve palsies, (c) Radiological
evidence of erosion of the base of the skull.
XII - Metastatic Tumours : 15 - 20 %
(a) Carcinomas of the lung, breast, stomach, prostate, thyroid and kidney are the
common sources of brain metastases.
(b) Usually met with in middle and late life.
(c) Secondary cerebral carcinomas are commoner than secondary sarcomas.
(d) Usually muliple, rounded, well defined, pinkish and rapidly growing.
(e) 4 th ventricular metastases present with morning headache, morning vomiting and
postural vertigo.
(f) Carcinomatosis of the meninges result in :
* multiple cranial nerve palsies.
* neck stiffness.
* headache.
* confusion and
* rarely subdural haematoma.
(g) Secondary melanotic sarcoma: may cause subarachnoid haemorrhage.
XIII - Tumours of Infective Origin:
1. Tuberculomas : commonly subtentorial (cerebellar) than supratentorial. A
tuberculoma consists of a yelow caseous centre surrounded by a pinkish-grey outer
zone . Calcification is frequent. Commoner in young age. Remissions and relapses
are common. A primary T.B. lesion elsewhere favours the diagnosis.
2. Gumma of the brain: is very rare and may start as a patch of gummatous meningitis.
Positive W.R.
3. Parasitic Cysts: may act as a space-occupying lesion e.g. hydatid cysts and
cysticercus cellulosae. Eosinophilia, and mononuclear pleocytosis in the CSF may be
present.
4. Brain Abscess: secondary to otitis media, pyaemia, or trauma.
93
CLINICAL PICTURE OF BRAIN TUMOURS
(A) GENERAL SYMPTOMS OF INCREASED ICT:
The classical triad of symptoms includes: headache, papilloedema, and vomiting.
This is present in only 60% of cases.
1. Headache:
* Paroxysmal at first, later continuous.
* Throbbing or bursting in character.
* More during the night and in the early morning.
* Increased by exertion, excitement, coughing, sneezing, vomiting, stooping and
straining at defaecation.
* It may be affected by the posture of the head.
* It is of a little localizing value, but usually subtentorial tumours give suboccipital
headache radiating down the back of the neck and may be increased by flexion of the
neck.
* Head ratraction may be present.
2. Papilloedema:
* Constant and severe in cerebellar, 4th ventricular, and temporal lobe tumours, absent
in 50% of cases of pontine and subcortical tumours, late in prefrontal tumours.
* Enlargement of the blind spot with concentric constriction of the field of vision.
* Progressive deterioration of the visual acuity.
* Post- papilloedemic optic atrophy and blindness may occur.
* Ipsilateral primary optic atrophy and contralateral papilloedema may occur in
olfactory groove meningioma (Foster Kennedy syndrome)
3. Vomiting:
* It occurs at night and in the early morning .
* It accompanies headache and may partially relieve it.
* It is not preceded by nausea except in children and not related to meals .
* Sometimes projectile in character.
4. Convulsions:
* Major fits occur in about 30 % of cases.
* Most common in cases of astrocytoma (68%), meningioma (60%) and glioblastoma
(51%)
5.Vertigo : A feeling of unsteadiness with a tendency to fall on stooping may occur.
6. Pulse : Acute rise of ICT causes bradycardia. Gradual increase in ICT causes
tachycardia.
7. B.P.: A rapid rise of ICT causes a rise in B.P. Chronic rise of ICT produces subnormal
B.P.
8. Respiratory Rate : Arapid rise of ICT with loss of consciousness produces slow and
deep respiration , or Cheyne - Stokes respiration A gradual rise of ICT unaffects the
respiratory rate.
9. Hypopituitarism : may occur due to downward pressure of the floor of the dilated 3rd
ventricle. Clinically : adiposity, genital atrophy, loss of body hair, hypoadrenalism and
hypothyroidism.
10. Somnolence: is met with in severe hydrocephalus due to hypothalamic affection.
11. Glycosuria: may occur.
12. Mental Symptoms:
* Acute rise of ICT produces coma.
* Subacute rise of ICT produces mental confusion with disorientation in time and space.
* Chronic rise of ICT may cause progressive dementia, or confusion, disorientation and
hallucinations.
* Rarely, excitement or depression may occur.
* Impaired memory with inability to concentrate and irritability are met with in mild
cases.
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* Mental symptoms are common in frontal lobe or corpus callosal tumours, or a result
of increased ICT e.g. in cerebellar tumours.
13. False Localizing Signs:
(a) Cranial nerve palsies : e.g. 6th nerve palsy and 3rd nerve palsy due to stretching of
the nerves and tentorial herniation.
(b) Bilateral extensor plantar responses.
(c) Bilateral grasp reflexes due to pressure by the dilated ventricles in hydrocephalus.
(d) Hypopituitarism due to downward pressure of the floor of the 3rd ventricle.
(e) Extensor plantar response on the same side as a hemispherical tumour due to
compression of the opposite cerebral peduncle against the tentorium.
(f) Cerebellar symptoms in frontal lobe tumours.
(g) Midbrain symptoms e.g. fixed dilated pupils, resulting from a vermal cerebellar
tumour.
(B) FOCAL SYMPTOMS: 1.
Frontal Lobe Tumours :
1. Prefrontal Tumours : (i.e. tumours anterior to the precentral gyrus).
(i) Headache is early, but papilloedema and vomiting are late or absent.
(ii) Mental symptoms may precede signs of increased ICT. They include : progressive
dementia with intellectual deterioration, stupidity, carelessness, urinary and faecal
incontinence, sometimes jocular, irritable, or depressed, (iii) Generalized convulsions
in about 50 % of cases with aura associated with speech (if
the tumour is near the base) or turning of the head and eyes to the opposite side with
toni-clonic movements of the contralateral limbs (in tumours near the superior aspect
of the lobe).
(iv) Catalonia (immobility in one attitude), or waxy flexibility, (v) Motor (expressive)
aphasia : due to involvement of the Broca's area, (vi) Grasp reflex in the opposite hand
and / or foot, (vii) Tonic perseveration (failure of relaxation after voluntary muscular
contraction) is a
rare sign of frontal lobe lesions . (viii) Contralateral hemiparesis most marked in the
face and tongue, due to compression
of the pyramidal fibres, (ix) Ipsilateral anosmia due to pressure upon the olfactory
nerve, ipsilateral primary
optic atrophy due to compression of the optic nerve, and contralateral papilloedema
due to rise of ICT are met with in olfactory groove meningioma and known as Foster
Kennedy syndrome. (x) Cerebellar symptoms may occur as
a false localizing sign .
2. Precentral Tumours: (i.e. tumours of the motor cortex)
(a) Pyramidal excitation: produces contralateral focal convulsions:
i. Typical Jacksonianfits : clonic movements of a focal onset e.g. in the thumb, march
course according to the order of representation of the body in the motor cortex, loss
of consciousness if the opposite side is involved. They are often followed by
temporary hepiparesis (Todd's paralysis).
ii. Partial Jacksonian attacks: limited to a small part of one side of the body and may
be continuous (epilepsia partialis continud).
iii. Serial Jacksonian epilepsy: frequent attacks up to several hundreds per day.
iv. Jacksonian status epilepticus with no recovery of consciousness between
successive attacks.
(b) Pyramidal destruction : produces contralateral monoplegia.
Parasagittal meningioma compressing the paracental lobules produces paraparesis,
retention of urine and impairment of position sense in the toes if the sensory area is
affected.
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Signs Associated with Localized Lesions
Location of Lesion
Prefrontal area
Frontal eye fields
Precentral gyrus
Superficial parietal
lobe
Angular gyrus
Broca's area
Superior temporal
gyrus
Midbrain
Associated Signs
Loss of judgment, failure of memory, inappropriate behavior, apathy, poor
attention span, easily distractible, release phenomena
Failure to sustain gaze to opposite side, saccadic eye movements, impersistence, seizures with forced deviation of the eyes to the opposite side
Partial motor seizures, jacksonian seizures, generalized seizures, hemiparesis
Partial sensory seizures, loss of cortical sensation including two-point discrimination, tactile localization, stereognosis and graphism
Agraphia, acalculia, finger agnosia, allochiria (right-left confusion)
(Gerstmann's syndrome)
Motor dysphasia
Receptive dysphasia
Early hydrocephalus; loss of upward gaze; pupillary abnormalities; third
nerve involvement-ptosis, external strabismus, diplopia; ipsilateral cerebellar
signs; contralateral hemiparesis; parkinsonism; akinetic mutism
Cerebellar
Ipsilateral cerebellar ataxia with hypotonia, dysmetria, intention tremor, nyshemisphere
tagmus to side of lesion
Pons
Sixth nerve involvement-diplopia, internal strabismus; seventh nerve involvement- ipsilateral facial paralysis; contralateral hemiparesis; contralateral
hemisensory loss; ipsilateral cerebellar ataxia; locked-in syndrome
Medial surface of Apraxia of gait, urinary incontinence
frontal lobe
Corpus callosum
Left-hand apraxia and agraphia, generalized tonic-clonic seizures
Thalamus
Contralateral "thalamic pain," contralateral hemisensory loss
Temporal lobe
Partial complex seizures, contralateral homonymous upper quadrant-anopsia
Paracentral lobule
Progressive spastic paraparesis, urgency of micturition, incontinence
Deep parietal lobe
Autotopagnosia, anosognosia, contralateral homonymous lower quadrantanopsia
Third ventricle
Paroxysmal headache, hydrocephalus
Fourth ventricle
Hydrocephalus, progressive cerebellar ataxia, progressive spastic hemiparesis or quadriparesis
Cerebellopontine
Hearing loss, tinnitus, cerebellar ataxia, facial pain, facial weakness, dysphaangle
gia, dysarthria
Olfactory groove
Ipsilateral anosmia, ipsilateral optic atrophy, contralateral papilledema
(Foster-Kennedy syndrome)
Optic chiasm
Incongruous bitemporal field defects, bitemporal hemianopsia, optic atrophy
Orbital surface frontal Partial complex seizures, paroxysmal atrial tachycardia
lobe
Optic nerve
Visual failure of one eye, optic atrophy
Uncus
Partial complex seizures with olfactory hallucinations (uncinate fits)
Basal ganglia
Contralateral choreoathetosis, contralateral dystonia
Internal capsule
Contralateral hemiplegia, hemisensory loss, and homonymous hemianopsia
Pineal gland
Loss of upward gaze (Parinaud's syndrome), early hydrocephalus, lid retraction, pupillary abnormalities
Occipital lobe
Partial seizures with elementary visual phenomena, homonymous
hemianopsia with macular sparing
Hypothalamus/
Precocious puberty (children), impotence, amenorrhea, galactorrhea, hypopituitary
thyroidism, hypopituitarism, diabetes insipidus, cachexia, diencephalic autonomic seizures
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II - Temporal Lobe Tumours :
1. Tumours of the uncus (the cortical centre for taste and smell, licking, mastication and
swallowing movements) may cause uncinatefits:
(a) Aura of gustatory and olfactory hallucinations, usually unpleasant.
(b) Involuntary licking, smacking the lips, or tasting movements.
(c) Dreamy state with a lapse of consciousness, but the patient does not fall.
(d) Amnesia for the attack afterwards, or deja vu phenomenon, or illusions e.g.
micropsia, macropsia, derealization, depersonalization (jamais vu), or fear and
depression.
2. Destruction of the uncus produces partial impairment of taste and smell on the
ipsilateral side.
3. Generalized convulsions may occur.
4. Bilateral partial impairment of hearing in tumours of the posterior part of the temporal
lobe (cortical hearing centre).
5. Tinnitus or auditory hallucinations.
6. Aphasia in left-sided temporal lobe tumours. Word deafness (inability to understand
spoken words) may occur. Jargon aphasia (voluble speech of meaningless phrases or
abnormal words) in severe cases. Apraxia may occur.
7. Visual field defects in about 50% of cases. A crossed upper quadrantic hemianopia is
characteristic, due to compression of the lower fibres of the optic radiation.
8. Neighbour hood symptoms: e.g.
(a) Weakness of conjugate deviation of the eyes to the opposite side.
(b) Pyramidal signs on the opposite side e.g. facial weakness.
(c) Partial ptosis and myosis due to affection of the ocular sympathetic.
(d) 3rd nerve palsy may occur.
(e) Diminished corneal reflex on the affected side (5th nerve compression).
HI - Parietal Lobe Tumours :
1. An irritative lesion of the postcentral gyrus (the principal sensory area) causes sensory
Jacksonianflts (paraesthesiae of tingling or electric shocks and rarely of pain) on the
opposite side of the body. Sensory Jackspnian fits may be followed by motor
Jacksonian fits if the precentral gyrus is involved.
2. A destructive lesion of the postcentral gyrus leads to sensory loss of the cortical type
(loss of postural sensibility, tactile discrimination, and astereognosis).
3. Hypotonia and wasting of the affected parts and both static and kinetic ataxia (sensory
ataxia in the finger-nose test) and pseudoathetosis may occur.
4. Thalamic over-reaction may occur in deeply seated parietal tumours.
5. Crossed homonymous lower quadrantic hemianopia due to compression of the upper
fibres of the optic radiation.
6. Alexia (inability to read) and agraphia (inability to write), with or without finger
agnosia and acalculia (inability to calculate) in lesions of the left angular gyrus.
7. Autotopagnosia (unawareness of the opposite half of the body) with neglect of objects
in the opposite half of extrapersonal space, in lesions of the right angular gyrus.
8. Ideational apraxia in lesions of the left supramarginal gyrus.
IV - Occipital Lobe Tumours :
1. Symptoms and signs of increased ICT are early e.g. headache
2. Convulsions in about 50% of cases with visual aura of flashes of light.
3.Visual field defects e.g. a crossed horaonymous hemianopia or a crossed homonymous
quadrantic defect, or a crescentic loss in the periphery of the opposite half fields.
4. Visual object agnosia and agnosia for colours in lesions of the left lateral occipital
region.
5. Neighbour hood symptoms e.g.
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(a) Alexia and agraphia due to compression of the left angular gyrus.
(b) Auditory hallucinations with word-deafness due to compression of the posterior
part of the temporal lobe.
(c) Impairment of taste and smell due to compression of the uncus.
(d) Cortical sensory impairment on the opposite side.
(e) Slight motor weakness on the opposite side.
(0 Nystagmus, hypotonia and inco-ordination due to cerebellar compression.
V - Tumours of the Corpus Callosum :
1. Mental symptoms are frequent e.g. apathy, drowsiness and memory defect with
progressive dementia.
2. Convulsions (major or focal fits) are common.
3. Double hemiplegia due to damage of both pyramidal tracts.
4. Grasp reflex unilateral or bilateral, due to extension of the tumour into the frontal
lobes.
5. Apraxia may occur e.g. left-sided apraxia due to interruption of fibres connecting the
left supramarginal gyrus with the right pyramidal tract.
6. Choreiform movements and tremors may occur due to compression of the corpus
striatum.
7. Signs of increased ICT are late.
8. CSF protein content is raised.
VI - Tumours of the Basal Ganglia :
1. Progressive spastic hemiplegia on the opposite side.
2. Sensory loss and sensory ataxia on the opposite side.
3. Homonymous hemianopia (affection of the optic radiation)
4. Somnolence.
S.Weakness of conjugate deviation upwards and inequality of puplis due to pressure
upon the upper part of the midbrain.
6. Signs of increased ICT develop rapidly when the 3rd ventricle is invaded.
Vn - Tumours of the Third Ventricle : may be:
(a) Intraventricular e.g. a colloid cyst, or
(b) Extraventricular e.g. tumours of the corpus callosum (above), of the basal ganglia
(laterally), or of the interpeduncular space (below).
Clinically :
1. Hydrocephalus : acute, subacute, chronic, or intermittent.
2. Paroxysmal headache which may be positional.
3. Papilloedema.
4. Progresive dementia, or coma may occur.
5. Pyramidal signs unilateral or bilateral (compression of internal capsule).
6. Amnesia.
7. Somnolence, polyuria, hyperglycemia, glycosuria, obesity, sexual regression and
irregular pyrexia may occur due to downward pressure upon the tuber cinereum and
pituitary gland.
VQI - Tumours of the Midbrain :
1. Internal hydrocephalus is early due to obstruction of the cerebral aqueduct causing
severe headache, vomiting and papilloedema.
2. Weakness of conjugate ocular deviation upwards with or without retraction of the
upper eye lid in upper midbrain tumours.
3. Weakness of conjugate ocular deviation downwards with or without ptosis and
weakness of convergence in lower midbrain tumours.
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4. Bilateral paralysis of the lateral conjugate gaze may occur in tumours just above the
pons.
5. Dilated unequal pupils with reflex iridoplegia
6. Nuclear ophthalmoplegia may occur.
7. Bilateral pyramidal signs with weakness, spasticity and hyperreflexia. Decerebrate
rigidity may occur.
8. Tonic fits with opisthotonos, extension of the 4 limbs and loss of consciousness may
occur.
9. Tremor, nystagmus and ataxia may occur due to damage of the cerebellar
connections.
10. Choreiform movements may occur.
11. Sensory loss due to affection of the long ascending sensory tracts.
12. Deafness, unilateral or bilateral due to compression of the lateral lemniscus.
IX - Pineal Body Tumours :
1. Signs of a midbrain lesion with early hydrocephalus as described above.
2. Macrogenitosomia praecox (of unknown cause).
3. Hypopituitarism and obesity may occur.
X - Tumours in the Region of the Optic Chiasma include :
1. Pituitary tumours.
3. Suprasellar meningiomas, &
Pituitary Tumours:
2. Craniopharyngioma.
4. Gliomas of the optic chiasma.
(A) Endocrine Disturbances:
1. Chromophil (Acidophil) Adenoma : causes hyperpituitarism with over production of
growth hormone leading to gigantism (if it arises before puberty) or acromegaly (if
arises in adult life), hyperglycaemia and glycosuria, thyrotoxicosis, hypertrichosis,
impotence in males and amenorrhoea in females and enlarged breasts with lactation
(excessive prolactin)
2. Chromophobe Adenoma : causes hypopituitarism leading to oligomenorrhoea or
amenorrhoea in females and impotence in males, soft skin with loss of hair e.g.
axillary and pubic hair, obesity, low metabolic rate, increased sugar tolerance,
hypothyroidism, hypoadrenalism, and hypogonadism.
3. Basophil Adenoma : may produce Cushing's syndrome with painful, plethoric
adiposity, cutaneous striae and purpuric patches, hirsutism, amenorrhoea,
hyperglycaemia, hypertension, polycythaemia & osteoporosis.
(B) Pressure Symptoms:
1. They may be absent in basophil and acidophil adenomas.
2. Headache, at first due to expansion of the sella (bursting and bitemporal) and later
due to increased ICT. Vomiting is absent or late.
3. Visual field defects :
(a) Bitemporal hemianopia usually asymmetrical, starting in the upper temporal
quadrant on one side.
(b) It may begin as a scotoma in the temporal half of the field.
(c) Complete blindness of one eye with temporal hemianopia in the other.
(d) Homonymous hemianopia occurs if one optic tract is compressed.
4. Primary optic atrophy, usually more marked on one side, but papilloedema is rare.
5. Ocular palsies due to compression of the 3rd or 6th cranial nerves and trigeminal
pain, sometimes with analgesia referred to the ophthalmic division of the 5th nerve.
6. Pyramidal signs, unilateral or bilateral due to compression of the cerebral peduncles
or of one hemisphere.
7. Uncinateflts due to compression of the uncus.
8. Mental changes due to compression of the frontal lobe.
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(C) Radiographic Findings: Expansion of the sella and thinning of its walls. Craniopharyngioma :
1. Endocrine Disturbances : due to compression of the pituitary and / or the tuber
cinereum resulting in adiposity or emaciation, polyuria, dwarfism, sexual infantilism,
or premature physical senility, or diabetes insipidus later in life.
2. Pressure Symptoms :
(i) Symptoms of increased ICT : Enlarged skull with separation of the sutures in
children, headache, vomiting and papilloedema.
(ii) Field defects due to compression of the optic nerves, chiasma, or tracts, (iii) Compression of frontal
lobes, temporal lobes and cerebral peduncles may occur.
3. Radiographic Findings : e.g. general signs of increased ICT, erosion of the clinoid
processes, flattening of the sella and calcification (suprasellar or intrasellar).
Suprasellar Meningioma:
1. It occurs in adult life.
2. Headache is slight.
3. No endocrine symptoms.
4. Visual field defects e.g. hemianopia, or a central, or temporal paracentral scotoma.
5. Primary optic atrophy .
6. Uncinate fits due pressure upon the uncus.
7. Generalized convulsions.
8. Hemiparesis.
9. X-ray skull may show erosion of the optic canal or clinoid processes, with flattening
of the sella and sometimes calcification.
Glioma of the Optic Chiasma : is rare.
1. It occurs in childhood.
2. Multiple neurofibromatosis may co-exist with it.
3. Primary optic atrophy with visual deterioration.
4. Visual field defects are bizarre.
5. Exophthalmos may occur.
6. No endocrine disturbances.
7. X-ray may show enlargement of the optic foramen and rarely enlargement of the sella
turcica forwards.
XI.- Cerebellar Tumours:
(A)Midline Cerebellar Tumours : e.g. Medulloblastoma.
1.
2.
3.
4.
5.
It affects children.
Early symptoms of increased ICT including headache, vomiting and papilloedema.
Enlarged skull with separated sutures.
Trunkal ataxia with little or no ataxia of the limbs.
Giddiness and unsteadiness with a broad-based gait and tendency to fall backwards or
forwards.
6. Muscular hypotonia.
7. No nystagmus.
8. Midbrain compression with tonic fits (extension of the limbs, opisthotonos, and loss
of consciousness), and the pupils may be dilated and slightly reacting .
9. Sixth and 7th nerve palsies may occur.
10. Weakness of the limbs, extensor plantar responses and sluggish reflexes (due to increased ICT) may
occur.
(B) Tumours of the Cerebellar Hemispheres : e.g.
Astrocytoma and cystic haemangioblastoma.
1. Early signs of increased ICT with suboccipital headache.
2. Nystagmus most marked on looking to the side of the lesion .
3. Ataxia of the limbs on the side of the lesion with clumsiness of the hand, positive
finger-nose and heel-knee tests and adiadochokinesis.
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