Download Athetosis

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Myasthenia
1ry ( Myasthenia gravis)
It is a disorder of transmission at the neuromuscular junction,
manifesting itself by easy fatigability especially on repetition of
movement &
by rest .
Aetielogy :
 Autoimm.
Ab IgG against receptors of A.ch at the
neuromuscular
junction . Ab released from B lymphocytes
defectively controlled by
T lymphocytes due to thymic gland
disorders.
C/P
12345-
6-
7-
>
 20 - 40 yrs
gradual onset progressive course
affects only the skeletal ms of the body
easy fatigue on repetition of movement
especial descending march
Ocular ms
ptosis , diplopia
Bulbar ms
dysphagia , hoarseness
UL then L.L ( pr. > D. )
Diurnal variation
The patient is more better in the morning, symptoms
increase as the day progress.
Some cases associated with
thyrotoxicosis
++ thymus gland
Investigation
1.
Induction of fatigue by a repetition of movement, also ask
the patient to count from 1-50 the words become less clear.
prostegmine test
I.m.
improvment
EMG
in amplitude of the waves with repetitive
2.
3.
movement
4.
CT Scan
for thymus ++
5.
Ms biopsy
6.
Antiacetylcholine receptors Abs
Q
Thymoma
mediastinal $
Aplastic anaemia (pure Red cell aplasia)
Bedside
test
38
Myasthemia gravis
* ttt
1.
medical
a prostegmine tablets 15 mg (anticholine esterase)
dose 1 tab. TDS
- Starts within 1/2 hr.
- peak 2 hr.
- duration 4 hrs
b pyridostegmins tablets. 60 mg
1 tab. TDS
- onset after 2 hrs
- 8 hrs duration
So we can combine a + b
 Ab
C Steroids - cytotoxic ( azathioprin )
d plasma pharesis ( remove Ab )
e I.V immunoglobulin
2.
Surgery
thymectomy
N.B.
 2 ry myasthenia = myasthenic $ (Eaton lambert’ $)
 It’s a paramalignant $
Myasthenia
 especial chch .
No march or diurnal variation
No response to prostegmine
 EMG
there is  amplitude with repitition
 ttt of the cause
 Neonatal myasthenia
offspring of myasthenic , give myasthenic
manifestation at birth, they recover within 2 - 6
wks
ttt


I.C.U. ( because of respiration distress)
plasma pharesis
 Toxic myasthenia
░ Botulism
░ Tick paralysis
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░ Aminoglycosides
░ Organophosphate
 Myasthenic Crises (Neglection of ttt)
 due to
 ttt
 A. ch. at the M.E.P
Prostegmine
Edrophonium (tensilon)
Severe weakness
Hypoventilation and
respiratory failure
 ventilation
 Cholinergic Crises
(Excessive ttt)
 d.t.  A. Ch. at the M.E.P
weakness and hypoventilation
 ttt
Atropin injection ± ventilator.
Myotonia
Def
voluntary
hand
mechanical
It is a delayed muscle relaxation after voluntary,
mechanical or electrical stimulation
when the pt. clenches his fist he is unable to open his
Tap the thenar eminence
adduction of thumb
The Myotonic phenomenon improved by repetition
of movement, warmth & worsened by cold
Types of myotonia :
Myotonia congenita
Myotonia atrophica
1- Herido familial
2- young age
3- Pseudo hypertrophy of
all ms
4- No dystrophic features
Sporadic
20 - 40 yrs
atrophy esp. of face &
sternemastoid
Dystrophic features
5- ECG changes
Rare types
Cataract Baldness testicular .
rare
ECG
+ ve
Myotonia paradoxica
(occurs with exercises)
40
M. acquisita (associated with  k)
ttt
Quinines - procainamid - Epanutin
41
Extra  system

It include all fibres that influence the motor activity & do not
pass
in the  tract

The centers situated at different levels ..
1- Cortical level
suppresser area in frontal lobe
2- Telencephalic level
Basal G.
3- Diencephalic level
thalamus & hypothalamus
4- Mesencephalic
Red N. & substania nigra in mid brain
All the previous centers form inhibitory circuit To Control the
discharge from the motor area
e. g. Cortical
caudate N.
G. pallidus
thalamus
this closed Circuit = Corticocaudato pallido-thalamo cortical
circuit which decrease discharge from motor area , so lesion
involuntary movement
function of extra  system :
1- Regulate & filter voluntary movement.
2- Regulate muscle tone
3- Regulate emotional movement
So , disturbance of function lead to
1- Hyper kinesia
2- Hypotonia or rigidity
3- Involuntary movement.
4-  regulation of associated movement
e.g. mask face
Parkinsonism
Shaking Palsy
It is a disturbance in the motor function characterized by slow movement,
muscle rigidity and tremors.
Causes: 1- Herido familial
wilson D
2- Symptomatic
post encephalitic
$
atherosclerosis
Neoplastic toxins
Reserpine, phenothiazins , Manganese
3- Idiopathic
=
paralysis agitans
42
Path
C/P
( dopamine esp . in substantia. nigra)
There is also depletion of pigmented neurones in the
idiopathic type.
James parkinson described 3 components
Tremors
Rigidity with hypokinesia
Hypokinesia
1- Static tremors
 Distal > proximal (first in fingers / thumb)
 Regular
 Rhythmic
 4-8 / sec. They are coarse tremors.
 increased with stress & disappear during sleep
 give the hand the pill rolling posture
2- Rigidity
● More in the proximal muscles
● Flexors more affected  gorilla like attitude
● Lead pips or cog wheel if interrupted by the
tremors
● Difficulty in starting the act of walking
 short stoppage gait
● Hypokinesia or bradykinesia.
3- Loss of emotional & associative movement
Mask
face
slow monotonus
speech
loss of swinging
of arm during walking
4- other associated manifestation
 Oculogyric Crisis
= Sudden Spasm of conjugated movement of
the eye mainly upward
 Greasy face
 autonomic disturbances e.g postural hypotension
 Glabellar reflex
normally tapping on the glabella produce blinking
which stops after 1st few taps, here it persist .
 Pt. Can’t resist propulsion & retropulsion

Micrographia (letters become small and
malformed)
43
No
No
No
No
Sensory (purely motor)
fasciculation
weakness ( brady kinesia or dyskinesia only)
sphincteric disturbances
Main types of parkinsonism
Post -encephalitic
paralysis agitans
atherosclerotic
any age
40 - 60 ys
> 60 ys
acute
Gradual
gradual
Regressive
progressive
Rigidity > tremors
tremors > Rigidity
Rigidity > tremors
+ve oculogyric Crisis
associated  signs
associated
associated with
coronary heart dis.

signs+hypertension
+ coronary
Treatment
N.B. there are 2 chemotransmitters in the basal
ganglia ( dopamine and Acetyl choline) which are in
balance
A. ch. which is
excitatory to movement.

tremors
So, parasympatholytics
drugs used in
parkinsonism
Dopamine which is
inhibitory to movement

Dopamine can’t
pass BBB

so give L – dopa
+ carbidopa
- Drugs used
1) Anticholinergic drugs (useful for tremors and rigidity but
not for hypokinesia)
 benzatropin (Congentin) 2 mg tab.
 parkinol
2 mg tab.
dose 1 tab. TDS
 tremaril
5 mg tab.
 Side effects :
1- Retention of urine
Q :value of percussion of lower abdomen in
parkinsonian patient (old age)
2- Tachycardia
3- Dryness of mouth
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4- Hallucination
 drug induced
parkinsonism ttt by anticholinergic
why ?!
 as dopamine receptors suppressed
so, dopamine will be ineffective.
2 L - dopa
 1 - 4 gm / d.
 It is transformed to dopamine peripherally which
can’t pass BBB.
 side effects :
1- psychosis
2- palpitation
3- GIT upset
4- chorea
3 Sinement
(L.dopa + carbidopa) mainly for hypokensia.
inhibit the peripheral decarboxylation
of L- dopa into dopamine So L — dopa will pass
through BBB .
dose :
tab. contains
250 mg dopa
10:1
25 mg carbidopa
4 Amantadin
100 mg / 12 hrs
 uptake of dopamine by the neurons and used
as adjuvant therapy.
5 Ms relaxant and BB e.g Inderal 30-60 mg/D
6 Surgery:(brain grafting) implantation of foetal adrenal gland
or midbrain  release dopamine
Investigations in parkinsonism

1- Serology for $
2- CT
Atypical clinical signs .
3- Tests for Wilson’s D e.g. caeruloplasmin and serum
cooper
45
Chorea
It is involuntary movement ch. ch. by
- static
- irregular
- proximal > Distal
- pseudopurposive
- Sudden jerky
- Dysrhythmia
Causes:
It’s ch.ch. by  dopamine in caudate N.
 Heridofamilial  Huntington’s chorea
 Symptomatic
Rheumatic chorea
post encephalitic
vascular
Toxic  chorea gravidarum
 Idiopathic  senile chorea
Rheumatic chorea
( sydenham’s chorea )
It’s one of the major criteria of Rh. fever, It’s associated with other
rheumatic manifestation in about 10% (but never with arthritis & ESR
)
- age :
- C/ P :
5 - 15
>
►Choreic movement
see above +
 the patient unable to keep his tongue
protruded unsupported by his teeth
 Grimacing
►Hypotonia
 Scaphoid hand when the patient stretches his arm Over
extension at metacarpaphal. & inter phalangeal joint
 The knee jerk is pendular
 Dancing gait
►Emotional instability
laughing
crying
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Clinical varities of Rh. chorea
1
2
3
4
5
ttt
usuall type (see above )
chorea gravis  choric movement interfere with speech & sleep
chorea mollis  paralytic d.t. severe hypotonia
Manical chorea  excitment
Chorea gravidarum  It’s Rh. chorea ppt. by stress
of pregnancy
This disease is self limited within 6 - 12 m., So the treatment
will control the symptoms during this period .
1- Rest
2- Haloperidol 3 mg TDS, It is antidopaminergic drug .
Huntington’s chorea


It’s a heridofamilial , auto. dominant (AD )
age 30 - 40 yrs
It’s a degenerative disease affecting
BG
frontal lobe
- C/P.
 Involuntary movement
 apathy - irritability
 Dementia
Investig
ttt
caudate N atrophy on MRI
 Pheonthrazines
 Genetic screening and counseling
 The abnormal gene is located on chromosome 4
47
Hemiballismus
Def. Severe violent, involuntary movement of large amplitude on one
side of the body more severe in the proximal muscles. It is similar
to
chorea
Etiology : subthalamic hage
Athetosis
Lesion in putamen B.G.
It is involuntary movement ch.ch. by
 Static
 irregular
 Dysrhythmia
 Slow snake like
 tone 
 Distal > proximal
Dystonia
degenerative
post - encephalitic
putamen and
corpus triatum
ch.ch. by: Irregular - slow sustained muscle contraction leading to
torsion or twisting like movement mainly in the trunk & proximal parts
of extremities.
Classification of Dystonia:
1. Focal Dystonia:
- Blepharospasm
Hemifacial spasm
- Oromandibular
Spasmodic tortocollis
2. Hemidystonia:
Twisting arm and leg on same side of body, with involvement of
trunk muscles
3. Generalized
Treatment of Dystonia:
A recent trend is injection of Botulinum toxin in the affected
muscles. It is a very expensive medication.
Q. (D.D. of tremors)
1) Park.
6) senile fine - No rigidity
2) familial < 25 - F.H. - respond to BB
4) Hyperthyroidism
7) flapping LCF = asterixis
5) Alcoholics
8) drugs e.g B2 agonists
48
Involuntary movement
1
2
3
4
5
6
Myotonia ? !
ms fibrillation  spontaneous contraction of single ms ffibers !?
Fasiculation 
chronic irritation of AHCs
Tremors
discussed + choreic & parkinsonian
Dystonia , athetosis and Hemiballismus.
Tics
Coordinated repetitive quick movement they represent
psychologically generated habit, in the form of stereotyped brief
movement in face and limbs
7 Myoclonus
Sudden contraction of restricted group of ms mostly in a limb . It
occurs in uremia , LCF
49
Ataxias
It is an Incoordination of voluntary movement in absence of motor
weakness
Cerebellar ataxia ( motor )
Causes of cerebellar ataxia
1 Friedreich’s ataxia
,
Maries ataxia
Heridofamilial ataxia
2 Congenital
3 vascular
4 Toxic
( cerebellar Ar. occlusion )
alcohol
Barbiturates
Hydantions
5 Neoplastic  Medulloblastoma
6 Demyelinating disease D.S
Tests for cerebellar ataxia
 finger to nose
we find decomposition
 finger to finger
of
movement
&
intention(kinetic)
 finger to Doctor finger
tremor & dysmetria
Why intention tremors as during flexion the extensors try
to contract at the same time ( incoordination )
 Dysdiadokokinesis;- inability to carry out alternating
movemenets
with rapidity and regularity (e.g. pronation &
supination)
 Rebound phenomenon
 Buttoning & unbuttoning  earliest sign
 Heel to knee
 Hypotonia , hyporeflexia but no weakness
 Staccato speech
biphasic
 Nystagmus
on fixation
horizontal
Rapid phase toward fixing point
● Gait:
▪ Unilateral lesion → staggering gait towards the lesion.
▪ Bilateral lesion → wide base gait
▪ Vermal or central lesion → trunkal ataxia.
50
Herido familial ataxia
gradual
onset,slowl
y
progressive
course
Bilateral
symmetrical
Types
Friedreich’s ataxia
selective
sphincters are intact
Friedriech`s ataxia
Marie`s ataxia
cerebellar lesion (bilateral)
post. Column lesion in S.C (bilateral)
pirepheral neuropathy
 lesion in s.c. (bilateral)
Maris’s ataxia
purely motor
Bilateral  lesion
Bilateral cerebellar lesion
Friedreich’s
Marie’s.
 1 st decade
 Reflexes are, lost
or 
( cerebellar , PN )
 loss of superf. &
deep sensation
 associated
2 - 3 decade
exaggerated
skeletal deformities conj.Hr.D.
* extra  lesions may
be associated
intact sensation
* mental impairment
51
Q.
what are the systemic diseases
1- SCD
2- pellagra
3- friedreich’s ataxia
4- M- ataxia
5- motor neurone disease
all these diseases are Bilateral , symmetrical +  lesion
starting form below upward in the spinal cord and the
sphincters usually intact.
Recent classification of heredofamilial ataxias:
 Friedreich’s ataxia
Aut. R
 Ataxia telangiectasia
Aut. R
 Olivo - ponto - cerebellar atrophy
aut. D ( ataxia,
spasticity, extra  )
52
Sensory ataxia
This is due to loss of deep sensation at any point in its pathway
1 P.N. ( D. neuropathy )
2 post. root (tabes dorsalis)
3 post. column (SCD,Tv. Myelitis) 4 thalamus ( thalamic $ )
5 medial leminscus ( Brain stem lesion )
tests of sensory ataxia
1. finger to nose
2. finger to finger
3. Rhombergism
normal but when patient closes his eyes he
can’t do that .
Vestibular ataxia
Lesion of vestibular division of 8th Cr. Nr.
- Causes
Meniere’s D.
Labrynthitis
Acoustic neuroma
-C/P
vertigo , tinnitus - deafness
Nystagmus
on fixation
horizontal
rapid phase away from fixing point
Q/ causes of lost ankle with preserved knee reflex ?
1) C- equina
2) SCD
3) P. neurepathy
4) freidrich’s
5) pellagra
Wasting of the small ms of the hand
 The small ms of the hand are supplied by C8 - T1
P.N
Causes of the wasting:
root
1 AHC lesions
Motor N.D.
 Gradual onset
 fasciculation
progressive
 purely motor
mus
AHC
Ant. sp. Ar
occlusion
Tv. myelitis
•
Polio.
 6m-2 yrs
acute onset

 fever
 acute
 loss dissociated sensory
acute
 no sensory less
 LL asymmetry
53
2 Anterior root & spinal Nr:
cx Spondylosis
2rys in cx area
cx pott’s disease
3 Lower brachial plexus lesion
Brith injury
thoracic inlet $
4 peripheral Nr. lesion.
pancost
tumors
cx.rib
All causes of neuropathy
Carpal tunnel $
5 Others
distal myopathy
Ischemia
Rheumatoid ( disuse atrophy )
Q.
D.D. of purely motor disease :
1- Motor N.D.
4- Maries ataxia
2- myathenia gravis
5- Myopathy
3- polio
Motor neurone disease
Def
It is a degenerative disease of gradual onset & progressive course
affecting the motor system only. 5% of cases are familial ( Aut. D chromosome 21 )

It’s may affect LMN or UMN or both

It’s an autoimmune disease or due to slow virus.
C / P. middle ags or old age
>
1) UMN






types
spinal cord affecting corticospinal tract.
Brain stem affecting corticobulbar tract.
☼ Spinal cord lateral sclerosis
Bilat.  lesion from below upwards  early
paraplagia
late  Quadriplegia
☼ Brain stem  corticobulbar lesion
UMNL of bulbar Cr. N.
= pseudobulbar paralysis
Sympt.
dysphgia , nasal regurge
dysarthria , hoarseness
Signs
palatal & pharyngeal
reflexes are exaggerated
54
2 LMN affecting
 S.C.  affecting AHC ( progressive ms atrophy )
affecting cx. & lumbar  signs
of LMNL in UL & LL
Hypotonia
Hyporeflexia
fasiculations
wasting
(d.t. chronic irritation
of AHCs )
 Brain stem
lesion in
nuclei(LMNL)=true bulbar paralysis
sympt. as above
signs
pharyngeal
lost
Cr.
Nr.
palatal
reflexes
&
are
3 Combined UMN & LMN = Amyotrophic lateral sclerosis
there are combined sympt. of LMNL & UMNL
UL
LMNL
weak, wasting
fasiculation
LL
UMNL
Hypertonia
Hyperreflexia
= Tonic atrophy
also mixed
UMNL + LMNL
but mainly
UMNL
N.B No sphincteric disturbances as it is a systemic disease
Investig & ttt:- - EMG (vit. , tonics , physiotherapy )
- Recently growth factors may be of value
Pseudo bulbar palsy
true bulbar palsy
- UMNL
- associated quadriplegia
- exagg. palatal & pharyngeal
reflexes
- jaw reflex may be
exaggerated ,if the lesion is
above pons
- Tongue
no wasting or
Fasciculation
LMNL
- ve
lost
- ve
small , flaccid,
& Fasciculation
55
Headache
* Def.
pain from the brows back to the suboccipital region
Pain sensitive structures are
Tissue covering
the cranium
* aetiology
meninges
dural &
cerebral vs
Intracranial
venous sinus
1 vascular headache
 Migrainous type
Hypertension
 Non - migrainous
coital
headache
during
intercourse
Vasodilators
2 space occupying lesions
▪Due to stretch of the meninges as in brain tumors.
The headache is worse on waking up and may awake
the patient from sleep.
▪The pain worsen on bending down and with
straining.
3 ms contraction headache
due to muscle spasm e.g. driving cervical
spondylosis
4
Meningeal irritation e.g.
meningitis, or by blood as
In subarachnoid haemorrhage
5 Tension headache ( very common )
This is usually associated with depression , anxiety
in the form of sense of pressure or bandage around
the head
6 Referred from
teeth
nasal sinus
eye , ear
56
Migraine
Def. It is a paroxysmal disorder ch. ch. by intense pain in the head ,
usually unilateral which preceded by visucal , sensory or
autonomic manifestation it may be bitemporal or generalized
° ♀ ≥ ♂, puberty
Aetiology
° Heridofamilial, recently a mutation on chromosome 19
was discovered
° urban area
° Hyperactive, obsessive personality.
° ppt by chocolate, smoking, alcohol stress.
C\P (The characteristic feature is the episodic nature)
1 prodroma
2 Aura
drowziness , hunger
immediately before attack
visual hallucination flaches of light
scotomatas
bright spot appear near the periphery
of the visual field which gradually expands
3 Headache
▪It starts in the temple or around the eye & spreads
to involve the whole side of the head , It is
throbbing
in character
▪It lasts for hrs or days associated with nausea , pallor
▪It passes away with sleep
Mech.  aura due to vaso constriction of intracranial vs
(carotid) & headache due to subsequent dilatation .
in the extra cranial arteries , Due to fluctuations
in blood 5 HT levels .
Types
1 classic migraine with aura
2 Common migraine
No aura
3 ophthalmoplegic migraine
paralysis of extra occular ms
57
4 Basilar m. occipital headache preceded by vertigo and diplopia
5 Hemiplegic m.
associated with hemiplegia
Cluster headache
There are attacks of severe headache starting on one side in the
Orbital & frontal region  spreading gradually to the same side
Association
lacrimation
conjunctival injection
Rhinorrhea
The attacks characterized by their regularity & occurrence in
clusters every 24 hrs for few wks or months , each attack ( minutes
to hour )
the clusters followed by long free periods ( 6m - 12 m )
*
ttt
of Migrain
1 During attack
Rest in dark quiet room
Ergometrine is the drug
of choice during attack
oral or subling
recently sumatriptan ( serotonine
agonist )
6 mg s.c injection
N.B Ergometrine may
lead to
-myocardial infarction
-abortion in
-Retinal artery
occlusion
Analgesics as paracetamol
Anti emetics as metaclopramide
2 In between attack
(If migrain attacks are frequent (e.g.
weekly)
to the frequency and intensity .
 avoid ppt. factors - stop contraceptive pills
 Indral
Inhibit V.D. 40 mg Tds (It can pass BBB)
58
 Cinnarizine ( stugeron )or sibelium ( Ca.Ch.B)
 Tegretol can be used or Epanutin
 Tryptizol small dose 25 mg/d at night
 Recently topiramate 25-100 mg (antiepileptic drug)
Cranial nerves
Olfactory Nr.
pathway of smell
Olfactory mucosa  fibers of olfactory N.
 cribriform plate  olfactory bulb
 olfactory tractolfactory sensory fibers in the uncus in temporal
lobe
Causes of unilateral anosmia
1- traumatic  fracture cribriform plate
2- Inflamm.  Basal meningitis
3- Neoplatic  tumors of the inferior surface of frontal lobe
Causes of Bilat. anosmia
Causes of parasomia
(perversion of smell)
ENT causes
Hysterical
Temporal lobe epilepsy
Herido familial
Psychic
Optic Nr.
Pathway of
vision
light reflex
accommodation reflex
Causes of optic Atrophy





Optic neuritis
secondary to papilloedema
Chronic glucoma
Optic Nr compression
F. ataxia
see the
practical
part
Causes of papiloedema





ICT
Central retinal V. obstruction
Malignant hypertension
Co2 retension
Cavernous sinus thrombosis
59
 Sarcoidosis
60
Oculomotor Nr.
The nuclei of this nerve are situated in the M. B. ,
Motor
to superior, inferior,
medial recti & inferior
oblique and levator palpebral superioris ms
Autonomic parasympatheric to sphincter pupillae& cilia
ms
lesion result in
diplopia complete ptosis
paralytic divergent squint
pupil . dilatation
paralysis of the ms supplied by the nerve
Trochlear Nr.
( So4 )
The nucleus is situated in the lower part of the M.B. , It supplies
the sup. oblique ms
 limitation of movement. of the eye on looking outwards ,
downwards toward the affected side
 diplopia
Abducent Nr
( LR 6 )
It’s nucleus is situated in the lower pons the nerve supply the lateral
rectus
the lesion
paralytic convergent squint
limitation of movement of the eye on
looking outwards towards the affected side
Pupil
The iris receives the following nerve supply
Parasumpathetic
through Cr. Nr. 3
sympathetic starts C8 , T1 from the
hypothalamus & descends through the
brain stem & spinal cord to L.H.C of C8T1
Argyll Robertson pupil
Miotic pupil , it’s reactive to accommodation & not to light
Causes
D. M. $
D. S.
Alcoholism , encephalitis
61
Syphilis (Tabes- Dorsalis)
62
Adie’s pupil :
 It is a heridofamilial
 It is
larger than normal
doesn’t react to light
React slowly to accommodation
Ophthalmoplegia
Def It is a paralysis of extrinsic & intrinsic ocular muscles.
I
Supranuclear ophthalmoplegia
Hge
thrombosis
embolism
unilateral lesion
No effect as ocular
Cr. Nr. are bilaterally
represented
II
Nuclear
III
Infranuclear
Ophthalmoplegia
we will enumerate
5 points
D.D.of miosis
Bilateral
paralysis on
both sides

 quadriplegia
 pseudo bulbar paralysis
unilateral lesion
S.&S. of brain stem lesion
causes
vascular
Neoplastic
inflammatory.
Degeneration
unilateral
all ms affected
Cr.Nr.
( e.g. D.M. )
1
2
3
4
5
Cr. Nr. 3 , 4 , 6 paralysis
Conj. eye movement paralysis
Ocular myasthenia
Ocular myopathy
Grave’s disease
1 pontine lesion
2 Argyll pupils
3 pilocarpine, chronic addiction
4 Horner’s
63
D.D. of mydriasis
1 Dark
3 Atropine
5 Dilated fixed pupil
D.D. of ptosis
1 mechanial
2 3 rd Cr. N.
4 M.B. lesion
oedem.
trachoma
2 Myathenia
4 Horenr’s
6 3 rd Cr. N. paralysis
3 Myopathy
5 Cong
7 Hysterical
Trigeminal nerve
1 Sensory division
It’s formed of 3 brs
ophthalmic
Maxillary
Mandibular
trigemenal nuclei
spinal N.
in the lower part
of M.O. & receives
pain & temp.
Mesencephalic N.
in the mid brain
& receives
deep sensation
Main sensory N.
receives
crude touch
Fibers from these nuclei ascend as trigeminal lemniscus with in
brain
stem to thalamus & then to cortical sensory area of
the face.
2 Motor division
It starts in the motor nucleus in the pons it supplies ms of mastication
Lesion of 5 th Cr. Nr.
1 Sensory
2 Motor
loss of conjunctival & corneal reflex
Hypothesia of the face ( same side )
 weak ms of mastication
 exaggerated jacoreflex
= ( Bilat.  tract above pons )
64
Trigeminal neuralagia
It’s ch.ch. by Severe attacks of pain along one or more of the
sensory branches of trigeminal nerve usually the mandibular & maxillary
divisions.
aetiology
C/P
ttt
Alcohol - D.M.
H. Z. infecton- aberrant loop of Ar compressing its rootlets
middle age 40 - 50 ys
- Severe brief lancinating paroxysms of pain lasting 1-2 min.
- The attack ppt. by movement of the jaws as chewing,
laughing , brushing of teeth
- No sensory loss
 analgesic
 Epanutin can be given
 carbamazipene ( tegretol ) 100-200mg TDS
 recently Topiramate 100 mg (Topamax)
Glossopharyngeal neuralagia
It is a pain occurs in throat, tonsillar fossa, the pain ppt. by
swallowing - No underlying abnormality can be detected.
ttt
carbamazipen ( tegretol )
D.D. of facial pain
1- 5th neuralagia
2- Sinusitis
3- Toothache
4- tempromandibular arthritis
5- Atypical facial pain ( Neurotic
)
65
fascial Nerve
The fascial nerve is a mixed nerve , 3 parts
motor part
Sensory part
Supplies the ms of
Receives taste
expression of the
from anterior 2/3
face 
of the tongue
- platysma
- post belly of digastric ms
Anatomy of 3 parts
see the practical part
lesion in fascial N.: it may be
UMNL
 affecting  tract
above facial nerve
 paralysis of the ms of lower
1/2 of the face on the opposite
side of lesion
 paralysis of voluntary
& spares the emotional
& associative movement
 Hemiplegia on the same
side of the paralysis
autonomic part
supplies
lacrimal gland
& sub maxillary
sublingual
salivary gland
LMNL
affecting the fascial motor
nucleus or the nerve itself
paralysis of ms of upper &
lower 1/2 of face on the
same side of lesion
paralysis of both movement
crossed hemiplogia
Causes of fascial n. paralysis
1 Causes of UMNL
facial paralysis see causes of hemiplagia
2 Causes of LMNL
facial paralysis
 In the nucleus
Infective  encephlitis
vascular

v. basilar
insufficiency
Neoplastic  Glioma
Demyelinating  D.S.
 In the cerebellopontine angle
middle ear disease
Bell’s portion
 In the extracranial portion
neuropathy
malignant
 G. B. $
of parotid gland
tumor
66
 D.M.
Causes of Bilateral fascial paralysis
1 Bilat. Bell’s palsy
4 G.B. $
2 Bilat. asoustic neuroma 3 D.S.
5 fascial myopathy or
6 Sarcoidosis
myasthenia gravis
Bell’s palsy
Def
It is an acute inflammation of the fascial nerve near to the
stylomastoid foramen ( labyrinthine part ) .
aetiolgy
there is relation ship to reactivation of herpes virus.
autoimmune !‫ – ؟‬cold exposure !?
C / P  acute onset of pain behind the ear then paralysis (LMNL)
there may be  taste on the ant. 2/3 of tongue !?
 Some pts describe the face as being numb !?
ttt
Nr.
N.B
A medical
Acetyl salicylic acid 4 - 6 g. / d.
steroids 40 - 60 mg / d. prednisolone
vit. B complex injection
B physiotheropy
Massage of the facial muscles
Galvanic stimulation to the ms
C Surgical
Grafting of the
Rarely used
Decompression
Gaurd against corneal ulceration by penicilline
ointment ( exposure keratitis )
Cochleo - vestibular Nr.
1 Cochlear division
fibres from cells of cochlea
pass from the inner ear through internal auditory canal
To cerebello - pontine angle
Relay in cochlear N. in pons
fibres ascend in lateral lemniscus of opposite side
 lesion
Tinnitus
Deafness
 causes
Acoustic neuroma
cerebellopontine angle tumor
67
meningitis
68
2 Vestibular division fibres from cells in vestibule of inner ear
join the cochlear division in the internal auditory
canal
To cerebellopontine angle
relay in vestibular N. in brain stem
New fibers take 3 pathways
archicerebellum M.L.B which is concerned with cerebral cortex
synchronous movement of
eye , head and neck
 lesion
Vertigo
Ipsilateral incoordination
Nystogmus
Vertigo
 It is the sense of rotation of the body in steady Surrounding or the
reverse
 It is an hallucination of movement of either the body or the
surrounding
+ vomiting , pallor & bradycardia
 causes
1 labyrinthine
physiological: sea sickness or motion
sickness
pathological
labyrinthitis associated
Meniere’s d
with
2 peripheral N.
acoustic neuroma
tinnitus
vestibular neuritis
3 Brain stem
vestibulo-basilar insufficiency
D. S. - encephalitis
4 Cerebral
 I.C.T.
5 psychogenic
It is termed giddiness & not vertigo
= instability in cases of anxiety
ttt 1- ttt of the cause
2- Betahistine (Betaserc). It is a histamine analogue.
3- Recently  stugeron ( ca. ch. blocker ) 25 mg TDS
N.B
vestibular function
 Caloric test
the ear is douched with H2O 7C above & 7C below
normal  Nystagmus for 2 m. if < 1 m = hypofunction
 Electro Nystagmography Recording nystagmus on a graph
69
Glossopharyngeal Nr.
1 Motor to  stylopharyngeus & superior constrictor.
2 Sensory to  pharynx - Tonsils - post. 1/3 of tongue
3 Taste from post . 1/3 of the tongue
Lesion
ipsilateral loss of taste & common
sensation of post. 1/ 3 of tongue
ipsilateral loss of pharyngeal reflex
Vagus Nr.
1 Motor to soft palate , pharynx , & lArynx
2 Sensory from
Skin over ext. aud. meatus
mucous membr. of GIT , resp. T.
Lesion
 Bulbar symptoms
Q True bulbar & pseudo bulbar see before
Accessory Nr.
It’s formed of 2 parts
1 Cranial part
2 Spinal part
Runs with the vagus & shares the
innervation of the soft palate & pharynx
Sternomastoid & trapezius
Hypoglossal Nr.
motor to the muscles of the tongue
1 U.M.N.L
 Deviation of the tongue to the opposite
 Side of lesion
e.g. capsular lesion
 No wasting or fasciculation
 If Bilateral
inability to protrude the tongue
2 L.M.N.L
 Unilateral  deviation of the tongue to the side of lesion
 Bilateral  Inability to protrude the tongue
70
 wasting & or fasiculation .
Aphasia
Inability of the formulation of speech in absence of lesions
of mental functions or sense organs .
Types
I. Sensory
(area 22 )
visual agnosia the pt. sees but doesn’t
recognize objects
Auditory agnosia
the pt. hears but doesn’t
understand sounds
( Broca’s )
II. Motor
(Exner’s area)
Agrophia
the pt. can’t express
his ideas in writing
area
verbal
the pt. understanding visual &
auditory stimuli , yet he
can’t express his ideas in
spoken words (expressive aphasia)
N.B. If a child is born deaf , he can’t initiate sounds & the
lack of speech in this case = mutism
Dysarthria
Difficulty in the process of articulation with normal formulation of
speech.
 Slurred speech
causes
 Bilateral  tract lesion
= pseudo bulbar paralysis
 lesion involving LMN
of Cr. Nr. or muscles concerned
with speech





true Myasthenia facial nerve
bulbar palsy
gravis
paralysis
Stacatto
cerebellar lesion
Monotonous
parkinsonism
Aphonia
Hysterical
lesion in vocal cord
Stuttering
= sudden interruption of the flow of speech or
repetition of sounds , It’s psychongenic
Scanning in combined  and cerebellum lesions
71
Brain tumors
Def: space occupying lesions in the cranial cavity, whether of
neoplastic or of chronic inflammatory origin ccc by:
1  I.C.T.
2 True localizing signs
3 False localizing signs
Classification:
1 Meninges
2 Brain tissues
= Gliomas
Meningioma (benign)
Astrocytoma
Medulloblastoma
(malignant)
3
4
5
6
7
Glioblastoma
Bl. vs
Hemangioma
Haemangioblastoma
Cr. Nr.
Acoustic neuroma
Pituitary tumors (benign)
Secondries
Cerebral
lymphomas
(malignant)
8
Space occupying lesion
simulating neoplasm include tuberculoma and
subdural haematoma.
Effects of tumors :
1 Tumor invade & replace brain tissue
2 Tumor compress tissue & blood vessels  ischaemia
3 New vessels formed in the tumor with no BBB characters
 bl vs with abnormal permeability
4
Obstruction
of
C.S.F.
pathway
ventricular dilatation
with compression of brain tissue
72
N.B.
The Bl. vs within the brain tumor lack the
characters of BBB, this  Brain edema around the tumor due
to abnormal permeability of these blood vessels.
C / P of brain tumor:
A- General S. & S. of  I.C.T.
I. Headache
due to stretch of meninges.
dullaching , bursting .
Its peak is in the morning , also
increased with cough &
sneezing .
It has no significant value in
localizing the site of the tumors.
 of V.C. in M.O.
 in the morning or during night.
not related to meals or
preceded by nausea.
projectile without efforts.
II. vomiting
III. papilloedema
important signs of  I.C.T.
Blurring of visions.
concentric contraction .
of the field of vision ( fogy )
B- False localizing signs
e.g. 



mainly due to  I.C.T.
6 th Cr. Nr. paralysis
As it has a long course in the cranial cavity
Dilatation of 3 rd ventricle
Compression of the optic chiasma &
pitutary gland.
Dilatation of 4 th v.
Compression on M.O.
 HR
due to compression on V.M.C.  BP
Lateral Ventricle
pressure on frontal lobe
73
C- True localizing signs
The signs depend on the site of the tumor
74
1 Frontal lobe tumors


Destructive lesions
 Motor , hemiplagia starts as monoplagia opposite the site
of lesion.
 Motor aphasia
 Conjugate deviation of the eye to the site of lesion
 Organic psychosis
 Forced grasp reflex
Irritative lesions
( focal epilepsy )
motor jacksonian fit
N.B.
Foster kennedy’s $
tumors of the frontal lobe may leading to
ipsilateral optic atrophy & contralateral
papilloedema .
2 parietal lobe tumors

Destructive

Irritative
contralateral cortical sensory loss
Apraxia (loss of ability to carry
out a movement on commend)
sensory jacksonian fit
3 Occipital lobe tumors

Destructive
hemianopia

Irritative


contralateral
homonomus
.
with macular sparing
visual hallucination
4 Temporal lobe tumors

Destructive

irritative
olfactory)hallucination
no effect on taste or
smell ( Bilaterally represented )
Mentality changes
uncinate
fit
(gustatory
&
75
psychomotor epilepsy
5 Pituitary tumors
 Hormonal manifestation
 chromophobe adenoma  hyperprolact .
 Acidophil adenoma  Gigantism or acromegally
 Basophil adenoma
 cushing disease
 Neurological manifestation
2 ry to compression of neighbouring structures.
optic chiasma
pituitary
- Anteriorly
optic chiasma
optic nerve
Brain stem - posterior
brain stem lesions
optic tract
- lateral
optic tract
- superior
Hypothalamus
 polyphagia
 Disturbed body temperature
 D. I.
 Hypersomnia
  ICT
N.B.
plateau waves
 in I.C.T. last for minutes , this caused by failure of
vascular autoregularity mechanisms of the I.C.T. & ppt by
sneezing , straining or
cough, It may be associated with
neurological manifestation .
6) Brain stem tumors
  I.C.T.
 Hemiplagia ( opposite side )
 Hemihypothesia ( opposite side )

M.B.
pons
medulla
Cr.Nr.
Cr.Nr.
Cr.Nr.
III-IV
5,6,7,8
9,10,11,12
Cerebello - pontine angle tumors
A The comment is the acoustic neuroma of 8 th cranial Nr it
may be bilateral in case of neurofibromatosis
b- Pontine glioma
c- Cerebellar tumors  medulloblastoma
C / P.1-  I.C.T. (as before)
2- pontine lesion (asbefore)
3- Cerebellar ataxia
Hemiataxia on the same side of the
lesion.
76
77
Pathology of brain tumors:
1- Meningioma
, from arachinoid villi
compresses without invasion
it may recur after removal
2- Glioma
They arises from supporting glial tissue of C.N.S. ,
a- Astrocytoma
 Mostly benign
 adult  cerebral
 child  cerebellum
b- Medulloblastoma
 Highly malignant
 common in children
and arised from
cerebellum.
3- Neurofibroma from schwanne cells of 8th Cr.N.
4- Craniopharyngioma from Rathke’s pouch , compress the
pituitary, and optic chiasma, Nr. & tract
It is common in children
Investigation
1 plain x - ray skull
 ICT
Separation of cranial sutures
Silver beaten appearance
++ of sella turcica
 Shift of calcified pineal body ( midline structure)
 Calcification in tumors as in meningioma and
cranio-pharygioma
Cerebral angiography: it may show displacement of
2
cerebral
vessels or abnormal vascularity
3 EEG
4 C.T. scan ( computerized tomography )
N.B
Contrast nephropathy may occur after C.T. as
sometimes we inject contract media I.V.
5 M.R.I
localized
ttt ..  Operable
No infiltration
good G. condition - accessible
Treated by Resection & deep x- ray therapy
78
 Inoperable
 Dehydrating agents
 Cytotoxic
 Radiotherapy
Dexamethazone, mannitol 15% I.V
glycerin oral
intrathecal Methotrexate
Cerebro vascular diseases
Cerebrovascular diseases include disorders of the arteriovenous
circulatory system leading to injury of the central nervous system. The
lesion (stroke) describes the functional neurologic injury.
pathophsiology of cerebral circulation :
1 The circle of willis provides a potential effective
anastomotic pathway
2 The circle loses some of its effectiveness because of
narrowing or absence of the communicating segments
3 There is  musculature esp. at point of exist of vessels
from the circle of willis  vulnerable points for
aneurysm
4 Absence of elastic tissue    incidence of
immunologic inflammatory disease
BBB ...
Insulate the brain & its extracellular fluid including
C.S.F. from many chemicals that affect the systemic
circulation .
the
Epidemiology :
1
3
5
7
9
55 yrs or more
2 Heart disease  embolism
Hypertension
4 M. infarction
Smoking
6 D . M.
Hypercholestrolemia
8 Pills
Collagen diseasevasculitis10 alcohol intake
Types of stroke :
1 focal stroke
caused by vascular occlusion or Hge
2 Global stroke
total failure of blood supply as in
cardiac arrest or Hypoxic states .
79
Findings suggesting cardiac origin for strokes:Z
1 Person < 45 yrs
2 Known heat Disease.
3 Emboli in other organs
N.B.
1 Most common Artery to be occluded with emboli is M.C. Ar.
2
Small infarcts
5 - 8 mm = lacunar infarction common in
hypertension
3 Hemmorrhagic infarction
scattered areas of escaped RBCs in the
ischaemic tissues surrounding infarction due to  pemeability to
RBCs (diapedesis)
4 There is also ischaemic edema at the surrounding area of infarction or
haemorrhage .
Important definitions of stroke
 Transient ischaemic attacks (TIAs)
 focal neurological
deficit for < 24 hrs
due to transient cerebral
ischaemia
 RIND
=
reversible ischaemic
but as TIAs for
about
neurologic defects
24 hs - 36 hs
 Stroke in evolution
in
condition where ischaemic neurologic deficits begin
focal or restricted zone but after hours , it progress to
affect enlarging zones
 Completed stroke
80
81
Transient ischaemic attacks
Def
It is a focal acute neurological deficit due to vascular insufficiency
lasting few minutes up to maximum 24 hs
Aetiology  spasm of artery due to thrombosis
 emboli which rapidly dissolve
C / P.
1 Risky pt. (see epidemiology )
2 focal manifest .
 Cr. Nr.
deviation of mouth
 speech
dysarthria
 sensory
hypothesia in U.L or UL + LL
 Motor
monoparesis or hemiparesis
Investigation





ttt
CT scan
normal
ECG , Bl. sugar ,serum lipids, fundus examination.
Bl. picture
to discover any risk factors
Angiography
for carotid vessels or
Duplex scan
vertebrobasilar systems
1 ttt of risk factors
2 Vasodilators
Control B.P.
Control Bl. sugar
Hypolipidemic drugs.
stugeron (ca. ch. blocker cerebral
V.D.)
acts on RBCs deformability  increase O2
delivery
4 Anticoagulants
as long as no contraindications as
3 Trental
old age!?
Severe hypertension
Bleeding
tendency
we give heparin 1000 unit/hr I.V drip for 1 wk
then oral warfarin tab. For 6-12 months, then
antiplatelets for life
5 Antiplatelets
aspirin or ticlopidine
 follow up to  further attacks & to  possibility
of stroke in the future
6 Carotid endarterectomy.
82


TIA of vertebrobasilar system
vertigo, diplopia,
ataxia and syncope
TIA of carotid often experience monocular transient
blindness (amaurosis fugax)
83
Vascular occlusive $
A
Internal carotid Ar. occlusion
 age
 sex
 onset
any age but commonly 4th - 6th decades
>
preceded by recurrent transient attacks of the
following
 Headache ,Aphasia.
 hemiparesis, & mental changes
= ( carotid T.I. As )
Complete occlusion
over
B
cap.
br.
 Ipsilateral blindness
 Contralateral hemiplagia
 Contralateral hemihypothesia  Mental changes
 Contralateral H. hemianopia  Aphasia
N.B.
the internal carotid pulse may be or bruit
it may be heard
Middle cerebral Ar. occlusion
cortical br. (supply face & U.L. )
Main stem
1 Capsular br.
( lenticulostriate Ar.) = the Ar. of hemiplagia
capsular hemiplagia (see before)
2 Cortical brs
 Fascio brachial monoplagia
 Cortical sensory loss in U.L.
 Auditory agnosia
 Motor aphasia
 Mental changes
3 Main stem
( middle cerebral Ar.)

contralateral.
hemiplagia
UL > LL
 contralateral hemihypothesia with cortical sensory loss in
U.L.
 Aphasia
 Coma
84
c
Ant. cerebral Art. occlusion
1 capsular br.
faciobrachial monoplagia as the fibres of the
face and UL are present in the anterior limb of internal capsule
2 cortical br.
 Mental changes
 Monoplagia in L.L.
 Cortical sensory loss in L.L.

Urinary
incontinence
N.B center of bladder in the medial surface of cerebral
hemisphere
3- Main stem
hemiphgia LL > UL with cortical sensory lossin LL
Apsaxia
d
Post. cerebral Art. occlusion
1 Cortical br.
2 Capsular br.
( supply occipital lobe)
H. hemianopia with macular sparing
= thalamogeniculate Artery
supply Caps. , thalamus , B.G.
= thalamic $
Thalamic pain on
opposite side
Hemihypothesia on choreoathetotic
to the opposite side movement
(as it supplies the
BG)
3 Main vs
H. Hemianopia with macular sparing
Thalamic $
Vertebro basilar insufficiency
I Vertebral Art.
Partial. occlusion
= insufficiency
complete occlusion
( Tr. isch.As )
e.g.
 syncope
 diplopia , opthalmoplegia
 deep coma
 bulbar paralysis
 respiratory paralysis
 bulbar sympt. + ataxia
II Cerebellar Ar. occlusion
superior cerebellar Ar
 ipsilateral cerebellar ataxia
 ipsilateral horner’s $
 ipsilaterlal deaf
anterior inferior cerebellar Ar.
as sup. Ar.

Iplsilateral
85
 ipsilateral hemihypothesia
5 , 6 , 7 , Cr. Nr. lesion
Post. inferior cerebellar Artery occlusion
This vessel Supplies the lateral aspect ot
oblongata and cerebellum



P.C

P.C

P.C

P.C

P.C

the
medulla
cerebellum
sympathetic chain




lemniscus
9
10
11
spinal nucleus of the 5th Cr. Nr.
12
spinal lemniscus
the  tract
& postrior column
i.e (Medial lemniscus)
are present in the midline
in medulla oblongata
C/P.
= Lat. medullary $
= $ of wallenburge
1- Syncope , hicoup , vomiting , vertigo

Horner’s
hemiataxia paralysis
palato - pharyngio laryngeal
L paralysis
loss of pain & temperature.
of the face
2- The posterior Column and  tract are intact as they lie in the middle
of
contralateral
Ipsilat.
loss of pain &
temperature of the body
due to lesion in the spinal
lemniscuss
86
medulla oblongata.