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37 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 39 ░ 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 44 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 46 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 tractolfactory 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 7C above & 7C 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 diseasevasculitis10 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.