Intensive Neurology 2021

Central Nervous System (CNS)

  • Brain:
    • Cerebral Hemispheres:
      • Two hemispheres (Right & Left).
      • Each composed of lobes with centers and tracts (motor & sensory).
        • Frontal Lobe:
          • Personality, emotional control, social behavior.
          • Micturition centers.
          • Voluntary motor control.
        • Parietal Lobe:
          • Language (speech).
          • Calculation, visual-spatial, constructional skills.
          • Memory centers, optic tract, somatic sensation.
        • Temporal Lobe:
          • Auditory centers.
          • Verbal memory.
          • Smell centers.
        • Occipital Lobe:
          • Visual centers.
    • Basal Ganglia:
      • Function of the extrapyramidal system.
    • Brain Stem:
      • Composed of midbrain, pons, and medulla oblongata.
      • Functions:
        • Contains all sensory and motor pathways.
        • Nuclei of cranial nerves (all except 1 & 2).
        • Some centers (respiratory, conscious, sympathetic chain).
    • Cerebellum:
      • Composed of lateral hemispheres, vermis, and flocculonodular lobe.
      • Function:
        • Coordination (balance) of peripheral and axial body.
        • Balance of eye and ear function.
  • Spinal Cord:
    • Composed of 31 segments.
    • Ends at level L1 as conus medullaris & cauda equina.
    • Transverse Section Components:
      • Gray Matter:
        • 2 anterior horn cells (motor nuclei).
        • 2 posterior horn cells (sensory nuclei).
        • Collections of cells for lower-order reflexes.
      • White Matter:
        • Afferent and efferent fibers of motor & sensory tracts.
        • Stabilizes the spinal cord.

Peripheral Nervous System (PNS)

  • Spinal nerves + Cranial nerves
  • Anterior horn cell of spinal cord segment → peripheral spinal nerve → neuro-muscular junction → muscle
  • Defect = Astereognosis + Agraphaesthesia

The Motor System

  • Components:
    • Pyramidal Tract (Voluntary Movements):
      • CST (Corticospinal Tract).
      • CBT (Corticobulbar Tract).
    • Extra-Pyramidal Tract (Involuntary Movements):
      • Function of Basal Ganglion.
  • CST (UMN):
    • Course:
      • Motor cortex → Posterior limb of internal capsule until the anterior 2/3 → midbrain → pons → medulla oblongata (decussates in lower 1/3) → spinal cord → anterior horn cells → peripheral spinal nerves 'lower motor neurons'.
  • AHC → Spinal segment → peripheral spinal nerve → neuro-muscular junction → muscle
  • Muscle reflex arch

Motor System Lesions

  • UMNL (Upper Motor Neuron Lesion) = CST lesion
  • LMNL (Lower Motor Neuron Lesion) = PNS lesion
  • UMNL vs. LMNL:
    • Inspection:
      • UMNL: Muscle bulk = normal (but mild atrophy due to disuse); no fasciculations.
      • LMNL: Muscle bulk = marked atrophy; positive fasciculations.
    • Tone:
      • UMNL: Hypertonia = spasticity (clasp knife spasticity).
      • LMNL: Hypotonia = flaccidity.
    • Power:
      • UMNL: Decreased.
      • LMNL: Decreased.
    • Reflexes:
      • UMNL: Hyperreflexia, ankle clonus (+), Babinski (+), Abdominal (-), Cremasteric (-), Anal (-).
      • LMNL: Hyporeflexia, ankle clonus (-), plantar reflex (-), Abdominal (-), Cremasteric (-), Anal (-).
  • Differential Diagnosis (DD):
    • UMNL:
      • CVA (Cerebrovascular Accident).
      • MS (Multiple Sclerosis).
      • MND (Motor Neuron Disease).
      • Space-occupying lesion.
      • Spinal cord lesion.
    • LMNL:
      • AHC = Poliomyelitis.
      • Spinal segment = radiculopathy.
      • PSN = GBS (Guillain-Barré Syndrome).
      • NMG = MG (Myasthenia Gravis).
      • Muscle = congenital muscle disease.
  • Note: Sudden onset of UMNL may lead to spinal shock, presenting with hypotonia and hyporeflexia.
  • Note: Muscle wasting + fasciculation + hyperreflexia + hypertonia = Mixed lesion.

Cerebellum Clinical Lesions

  1. Types:
    • Cerebellar ataxia
    • Sensory ataxia
    • Vestibular ataxia
  2. Causes:
    • Congenital:
      • Friedreich's ataxia
      • Spinocerebellar ataxia
    • Structural:
      • Brain tumor
      • Abscess
    • Toxic:
      • Drugs (lithium, phenytoin, amiodarone, toluene, 5-fluorouracil, cytosine arabinoside)
      • Alcohol
      • Heavy metals/chemicals (mercury, lead, thallium)
    • Infection/Post-infectious:
      • HIV
      • Varicella zoster
      • Whipple’s disease
    • Degenerative:
      • Multiple system atrophy
      • Creutzfeldt–Jakob disease
    • Inflammatory/Immune-mediated:
      • Multiple sclerosis
      • Gluten ataxia
      • Paraneoplastic ataxia
      • Hashimoto encephalopathy
    • Metabolic:
      • Vitamin B1 or E deficiency
      • Hypothyroidism
      • Hypoparathyroidism
    • Vascular:
      • Stroke
      • Vascular malformations
      • Superficial siderosis
  3. Clinical Abnormality:
    • Face:
      • Head nodding & titubation
      • Dysarthria = Staccato, scanning, explosive speech
      • Horizontal nystagmus
    • Upper Limb:
      • Finger-nose test = intention tremor & dysmetria
      • Rapid alternating movements = dysdiadochokinesia
      • Rebound test = overshooting
      • +/- Hypotonia & pendular reflex
    • Lower Limb:
      • Heel-shin test = impaired
      • Gait = ataxic gait
      • Romberg sign = positive

The sensory system

  • Speech abnormalities
    • DD of dysphasia :
      • Brocs dysphasia
      • Wernickes dysphasia
    • DD of dysarthria:
      • Staccato speech = ataxia, MS
      • Slurred speech = CN 5,7,12 palsy (MND, MG)
      • Monotones speech = parkinsonism
    • DD of Dysphonia:
      • RLN injury
      • Vocal cord lesion
  • Posterior(dorsal) columnsensory tract
  • Spino talamic (anterior lateral) sensory tract

Site of Lesion and Motor/Sensory System Effects

  • Cerebral Hemisphere:
    • Motor: Contralateral hemiplegia or paresis (UMN in UL & LL)
    • Sensory: Contralateral sensory loss of face and body
  • Brain Stem:
    • Motor: Contralateral hemiplegia or paresis (UMN in UL & LL)
    • Sensory: Ipsilateral sensory loss of face, contralateral sensory loss of body
  • Hemicut above C5:
    • Motor: Ipsilateral hemiplegia or paresis (UMN in UL & LL)
    • Sensory: Complete cut above C5 results in DEAD
  • Hemicut C5-T1:
    • Motor: Ipsilateral hemiplegia or paresis (LMNL in UL, UMNL in LL)
    • Sensory: Complete cut C5-T1 results in quadriplegia or paresis (LMNL in UL, UMNL in LL)
  • Hemicut T1-L1:
    • Motor: Ipsilateral monoplegia or paresis (UMNL in LL)
    • Sensory: Complete cut T1-L1 results in paraplegia or paresis (UMNL in LL)
  • Hemicut Below L1:
    • Motor: Ipsilateral monoplegia or paresis (LMNL in LL)
    • Sensory: Complete cut below L1 results in paraplegia or paresis (LMNL in LL)
  • If Hemi cut : ipsilateral PCS lost & contralateral STT lost (brown squared syndrome) below site of lesion
  • If complete cut : complete sensory lose below site of lesion

Spinal Cord Lesions

  • Causes:
    • Spinal compression.
    • Postural trauma.
    • Inflammation (transverse myelitis).
    • Neoplasm.
    • Artery (ASA thrombosis).
    • Lesions of degeneration (Friedreich's ataxia, Vit B12 deficiency, myelopathy, syringomyelia).

Cerebrovascular Accident (CVA)

  • Anatomy:
    • Brain supplied by two main systems:
      1. Carotid system:
        • ICA → ACA & MCA → supply cerebral hemisphere.
      2. Vertebral basilar system
    • Each artery supplies a part of the brain:
      1. Anterior Cerebral Artery (ACA): Supplies the frontal lobe.
      2. Middle Cerebral Artery (MCA): Supplies the temporal and parietal lobe.
      3. Posterior Cerebral Artery (PCA): Supplies the visual centers.
      4. Basilar Artery: Supplies the brain stem and cerebellum.
    • Note:
      1. Motor involvement:
        • ACA → L.L > U/L & face.
        • MCA → U/L & face > L.Limb.
        • PCA → face & U/L > L.limb.
      2. Sensory involvement: Contralateral hemisensory loss.
  • Definition: Acute Focal neurological defect due to a vascular cause.
    • Types:
      • Ischemic CVA (85%):
        • Embolism is the most common cause (heart = A.Fib).
        • Thrombosis.
        • Hypotension.
        • Arteriosclerosis.
        • Vasculitis.
        • Space-occupying lesion.
        • Risk factors:
          • Hypercholesterolemia.
          • Uncontrolled HTN & D.M.
          • Obesity = high LDL.
          • Smoking.
          • Lack of exercise.
          • Alcohol.
          • OCP.
          • Homocysteinemia
      • Hemorrhagic CVA (15%):
        • Epidemiology:
          • 3rd most common cause of death in developed countries.
          • Common in Black populations.
          • Age > 40.
          • Male > Female.
  • Duration of Symptoms:
    • Transient Ischemic Attack (TIA): Acute focal neurological defect due to a vascular cause lasting < 24 hours.
    • Stroke: Acute focal neurological defect due to a vascular cause lasting > 24 hours.
  • Clinical Presentation:
    • ACA Occlusion:
      1. Contralateral hemiplegia or paresis.
      2. Contralateral hemisensory loss (L.L > U/L & face).
      3. Emotional changes.
      4. Behavioral & personality changes.
      5. Urine incontinence.
    • MCA Occlusion:
      1. Contralateral hemiparesis or plagia.
      2. Contralateral hemisensory loss (UL & face > LL).
      3. Auditory & smell disturbance.
      4. Aphasia.
      5. Impaired memory: Especially visual spatial memory, calculation, constructional skills.
      6. Contralateral homonymous hemianopia.
    • PCA/Basilar Occlusion (Brain Stem Infarction):
      1. Contralateral hemiparesis & hemiplegia.
      2. Contralateral sensory loss of (UL > L.L) of body.
      3. Ipsilateral sensory of face.
      4. Ataxia (cerebellum lesion).
      5. Cranial Nerve palsy (7, 9, 10, 11, 12).
      6. Visual hallucination & visual loss.
      7. Horner syndrome.
      8. Respiratory failure type II.
      9. Locked-in syndrome (loss of consciousness, can move eyelid).
  • Stroke Variants:
    • Minor Stroke: Symptoms > 24 hours but resolve without significant defect.
    • Progressive Stroke (Stroke in Evolution): Symptoms worsen due to increasing size of infarction.
    • Complete Stroke: Rapid, maximum, persistent neurological defect within a few hours due to multiple emboli.
      • Source of embolism is the carotid artery, affecting MCA & retinal artery.
    • TIA Evaluation: Any patient with TIA should undergo Doppler-Duplex U/S.
      1. Amaurosis fugax
      2. Auscultation (Carotid Bruit not always present).
  • Lateral Medullary Syndrome:
    1. Ipsilateral ataxia.
    2. Ipsilateral Horner's syndrome.
    3. Ipsilateral CN 5, 9, 10, 11 involvement.
    4. Contralateral STT sensory loss.
  • Differential Diagnosis of CVA:
    1. Hypoglycemia.
    2. Space-occupying lesion.
    3. Encephalitis.
    4. Epilepsy (Todd’s palsy).
    5. Peripheral neuropathy.
  • Horner's Syndrome:
    1. Partial ptosis
    2. Miosis
    3. Anhydrosis
    4. Enophthalmos

CVA Investigations

  • To Confirm Diagnosis (According to Site):
    • CT without contrast: Sensitive in detecting strokes due to ACA & MCA occlusion; aim is to exclude hemorrhagic CVA, as changes of infarction need 48 hours to appear. HRCT scan can show changes in 12-36 hours.
    • MRI: Sensitive in detecting strokes of the brain stem & cerebellum due to occlusion of basilar & PCA; also used to exclude hemorrhagic CVA.
  • To Detect the Cause:
    • Labs:
      • Blood sugar
      • CBC: Polycythemia & thrombocytosis
      • WBC, ESR, & CRP: Due to clot or vasculitis & SLE
      • Antinuclear Ab: When suspecting vasculitis due to SLE
      • RBS
      • Lipid profile
    • Imaging:
      1. Chest X-ray: For aspiration pneumonia.
      2. ECG.
      3. Doppler U/S of carotid artery: Both after stabilization of patient.

CVA Complications

  • Chest infection → Most Common Cause of death.
  • Epilepsy & dementia.
  • DVT & Pulmonary embolism (2nd cause of death).
  • UTI & Constipation.
  • Depression.
  • Painful shoulder.

CVA Management

  • Initial Steps:
    • DO MRI or CT scan
      • Hypo dense (Infarction)
      • Hyper Dense (White lesion)
    • Neurosurgeon Consultant (
    • Admit the patient
    • Primary Survey (A, B, C):
      • A: Patent airway.
      • B: Breathing, give patient 60% of O2 for the brain.
      • C: Circulation, insert 2 large cannulas and send blood for investigations.
      • Measure BP: If hypotension, give IV fluids (5% dextrose saline), but don’t over-hydrate (cerebral edema).
      • NGT insertion: For gastric lavage & prevent aspiration pneumonia.
      • Insertion of urinary catheter.
  • Prevent Further Stroke:
    • Aspirin 75mg + Dipyridamole 200mg.
    • Control DM: Soluble insulin by Sliding Scale.
    • Control BP: Transient HTN seen after stroke usually does not require Rx, but if BP > 230/100 mmHg or end-organ damage, gradually lower BP to 160/90. Anticoagulant is C/I.
    • Lipid-lowering agent (statin or omega-3).
    • Control Risk Factors.
    • Physiotherapy + Rehabilitation: Decrease complications & improve prognosis.
  • Thrombolytics:
    • Given with caution & only if no contraindications.
    • Not given > 4 hours because higher doses are needed, which may lead to rupture → Hemorrhagic CVA.
  • Note: Ischemia may lead to fever, which in turn will lead to increase infarction size.
  • Indications for Anticoagulant in Stroke:
    1. Atrial Fibrillation
    2. Stroke in evolution
    3. Recurrent TIA
  • Blood sugar monitoring is important to exclude DM.
  • Before considering management of ischemia, you must exclude hemorrhage.

Management of TIA (Recurrent 30%)

1.  Aspirin 75mg for life.
2.  Treat the risk factors.
3.  Regular Duplex U/S of carotid vessels; if >70% occlusion, stent is required.

Hemorrhagic CVA

  • Differential Diagnosis:
    • Sunstroke
    • Subarachnoid Hemorrhage
    • Hypoglycemia
    • Drug addict
  • Types & Causes:
    • Subarachnoid Hemorrhage:
      1. Rupture of saccular aneurysm
      2. Berry aneurysm
      3. A-V malformation
        • Idiopathic = hereditary hemorrhagic telangiectasia / PKD
    • Intracranial Hemorrhage:
      1. Rupture of micro B.V.
      2. Buchard Charcot B/c HTN.
  • Clinical Presentation:
    • Subarachnoid Hemorrhage :
      • Vomiting.
      • Blurred vision due to papilledema.
      • Irregular respiration.
      • Neck stiffness & occipital Headache.
      • Coma
    • Intracranial Hemorrhage :
      • Vomiting.
      • Blurred vision due to papilledema.
      • Irregular respiration.
      • Neck stiffness & Frontal Headache.
      • Coma
  • Diagnosis:
    • CT or MRI (sensitivity 75%)
    • Lumbar puncture:
      • Xanthochromia after 12 hours (yellowish pinkish CSF) & lasts for 2 weeks.
    • ECG: ST-segment elevation
  • Treatment:
    • Bed Rest.
    • Control BP gradually.
    • Dexamethasone & Mannitol.
    • Urgent neurosurgery consultant call

Intracranial Mass Lesions

  • Causes:
    1. Hematoma
    2. Infective
      • Cerebral abscess (pyogenic, Toxoplasma)
      • Tuberculoma
      • Hydatid cysts
    3. Granuloma
      • Sarcoid mass
    4. Neoplastic
      • Benign and malignant
  • Clinical Features:
    1. Local effects on adjacent brain tissue
      • Seizures
      • Focal signs
    2. Raised intracranial pressure:
      • Headache(Frontal ,early morning, increased by staring, coughing,bending ,wailking)
      • Impairment of conscious level
      • Papilledema
      • Vomiting, bradycardia, arterial hypertension
      • False localizing signs 6th cranial nerve lesion (unilateral or bilateral)
      • Bilateral extensor plantar responses
  • Investigations: * If there is no CT or MRI fundoscopy papilledema. * cranial nerve palsies, particularly CN VI (lateral rectus because it has a long intracranial root
    1. CT ( 1st to be done) or MRI
    2. CBC, ESR, CRP may be normal
  • NB: Lumbar puncture is CI because there is high risk of herniation ( conning)
  • Differential Diagnosis of neck stiffness:
    1. Subarachnoid hemorrhage.
    2. Meningitis.
    3. Disc prolapse or subluxation.
    4. Posterior fossa tumor.
    5. Migraine.
    6. Severe upper lobar pneumonia.
  • Treatment:
    Decrease intracranial pressure by giving manitol & dexamethasone & Rx cause

Benign Intracranial Hypertension (Pseudo tumor cerebri)

* This condition usually occurs in obese young women. without a space-occupying lesion (Exclusion Dx)
* The condition can be precipitated by drugs, including tetracycline, and vitamin A and OCP.
* **CP:**
1.  Headache, sometimes accompanied by
2.  Transient diplopia & visual disturbance
3.  Papilledema
4.  6th cranial nerve palsy may also be present (False localizing sign).
*   **Investigations**
1.  Lumbar puncture which shows raised CSF pressure,
2.  CT OR MRI = normal-sized or small ventricles.
3.  Visual perimeter is indicated to monitor the progression of disease.
*   **Rx:**
1.  Rx any precipitating condition(Decrease weight)
2.  Acetazolamide(Diuretics)3- Repeated LP

Multiple Sclerosis

  • Definition: Multiple neurological sclerosing defect separated by space & Time (R&R 80%).
  • Causes: Demyelination of white matter of CNS.
    1. T-lymphocyte mediated autoimmune response
      • Female > Male (20-40 yrs).
      • +ve F/H (Caucasians).
      • HLA Dr2.
      • Ab in CSF  oligoclonal band IgG 80%
    2. Post Viral infection (Measles), Ag-Ab  2ry Ab in CSF.
    3. Hot Climate → C/P exacerbation during hot bath (Utthoff's symptoms).
  • Clinical Picture:
    1. Optic Nerve (Most common site):
      • Painful unilateral optic neuritis (Intraocular Ophthalmoplegia), start unilateral then bilateral (increased by eye movement).
      • Diplopia: Due to optic neuritis → decreasing in propagation of single image less than other eye.
      • Impaired color vision (Rods & Cons).
      • D/D: 1- M.S 2- Vit B12 Def 3- Transverse Myelitis 4- sub-acute sclerosing pan encephalitis.
      • CI if evidence of high ICP
    2. Brain:
      a/ Motor: UMNL Mono progress to- Spastic Hemiplegia or paresis contralateral.
      If frontal lobes are affected bilateral pts may have paraplegia progress to quadri
      b/ Sensory: PCS Deep & Fine.
      Parasthesia and tingling sensation, radiating on arms back legs on flexion of pt. neck due to dorsal column Nuclei involvement. BARBER’S CHAIR OR LERMITTS SIGN.
      c/ Cerebellum: dystaxia and other cerebellar sign. Charcot triade (Nystagmus , tremor & Scanning speech)
      d/ Frontal: Euphoria or depression (emotional labiality)
      e/ brain stem: CN palsy especially CN3+4+6,(Diplopia)CN 5(trigeminal neuralgia), CN7, CN 12 (dysarthria)
    3. Spinal Cord:
      a/ Sub-acute degeneration of spinal cord b/ Urinary Dysfunction: Sphincter disturbance incontinise (Common in male)
  • Investigations:
    1. Visual Evoked potential: (delay) used for Subclinical Dx.
    2. MRI: 1st and most sensitive (White abnormal patches).
    3. Lumbar Puncture: mild T – Lymphocyte (Pleocytosis) . Protein. Oligoclonal band: IgG 80%
      • CT scan
    • Rx:
    1. Acute Relapsing:
      1/Steroid ((methyl prednisolone)) 1mg-IV x 3days. 2/Rx Complication.
      3/Vit B12.
    2. For prevention of relapsing:
      1/interferon beta (DOC)
      2/Azathioprine: decrease progression not cure
    • Common causes of optic disc swelling
      Raised intracranial pressure (papilloedem) 1-Cerebral mass lesion (tumour, abscess) 2-Obstructive hydrocephalus 3-Idiopathic intracranial hypertension Obstruction of ocular venous drainage
    • 1-Central retinal vein occlusion
      2-Cavernous sinus thrombosis Systemic disorders affecting retinal vessels 1-Hypertension 2-Vasculitis 3-Hypercapnia
      Optic nerve damage
      1-Demyelination (optic neuritis) 2-Leber’s hereditary optic neuropathy 3- Anterior ischaemic optic neuropathy 4-Toxins e.g. methanol, Hypocalcemia 5-Infiltration of optic disc 6-Sarcoidosis 7-Glioma 8-Lymphoma
    • Prognosis:
    • good30% = 10yrs50% = 15yrs.
      Poor prognostic factors: *Progressive type. *Frequent relapse. *Male. *Age>40 or <20.*Motor and cerebellar presentation
    • Optic atrophy

Motor Neuron Disease (Lateral Amylotrophic Sclerosis)

  • Definition: Progressive disorder of unknown etiology which results in degeneration of Cranial Nerve Nuclei, AHC, & pyramidal tract.
  • Causes: Unknown etiology but theories may be:
    1. Autoimmune: rare Disease common in male, > 40 yrs not ass’ with other autoimmune
    2. Trauma: Blunt or electrical.
    3. Toxins
    4. Post-viral infections
  • Clinical Presentation:
    1. S&S of UMNL & LMNL:
      Cranial Nerve Nuclei & AHC.
      Pyramidal tract + Betz Cells. -LMNL. -Msc wasting & fasciculation.
      -UMNL. - Reflexes
    2. Cranial nerve involvement (s&s of bulbar & pseudobulbar) difficult in
      Speech (Dysarthria). - Swallowing (Dysphagia) Aspiration pneumonia (MCC of death)
    • Rarely urinary dysfunction.
      • Common Presentation of MS: 1-Optic Neuritis & 6th CN palsy (False Localizing Sign) 2-Spinal cord lesions. 3-Brain stem lesions. 4-R&R Sensory lesions. D/D 1-Cervical cord compression (tumor, disc) 2-Late in Syringomylia 3-Sub-acute degeneration of spinal cord
        • if the patient complained of UMNL & LMNL at same limb it’s called ((Mixed Lesion)).
  • DD of mixed lesion:
    1. Motor Neuron Disease.
    2. Spinocerebellar Ataxia.
    3. Syringomyelia.
    4. Cervical myelopathy.
    5. Vit B deficiency
    • No exact Inv but CT & MRI to exclude other D/D
  • Treatment:
    1/Rilazale (Glutamate antagonist) which improve symptoms. 2/Rx complication. Prognosis: poor prognosis Fatal in 5-7yrs

Gullain Barre Syndrome

  • Def: Acute inflammatory ascending poly neuropathy Post infections 1-4 weeks ( CMV+EBV URTIs= Dyspnea) (Campylobacter Gastro enteritis= Diarrhea)
  • C/PPolyneuropathy (motor, CN involvement & Sensory)
    1/Motor Affect Muscles (LMNL). Lower Limb > Upper limb (Distal to proximal).
    Pts complain of fatigability difficulty from raising from sitting position or climbing stairs S&S of LMNL (Loss of Reflexes).
    2/Cranial Nerves Involvement: 7th (Bilateral), 3th, 4th, 6th & also bulbar Complaining of (Diplopia, Drooling saliva, regurgitation& dysphagia).
    3/Sensory: Parasthesia & Numbness (Distal to proximal) LLUL.
    4/Spinal Cord: Urinary symptoms (Retention). 5/Dyspnea: Late in course suggestive of diaphragmatic & intercostal Muscle Weakness RFII Death. may occur within hours of presentation
  • Inv: 1/Nerve conduction studies: Abnormal (Confirm Dx). 2/Electromyogram (EMG): Normal.
    3/CSF: Albumin-Cytology Dissociation ( High Protein & normal cells +Sugar) 4/Identify the Underlying cause: Stool Analysis & Bronchoalveolar lavage.
    5/Spirometer & ABG to moniter lung function
  • No 1-Sensory Loss. 2Ocular impairment. 3Cerebellar or extrapyramidal sign. 4Disturbance of level of consciousness. - Rx: 1/High dose IV gamma globulin during acute phase to reduce symptoms Plasma phoresis or exchange (Useful in Rx 1st week). 3/Ventilator support if respiratory Muscle is affected. 4/physiotherapy & occupational. 5/Vit B12 N.B: steroid has no role b/c no further formation of Abs

Polyneuropathy

  • Causes of polyneuropathy
    * 1-Genetic:Charcot–Marie–Tooth disease, Familial amyloid polyneuropathy, neuralgic amyotrophy
    * 2-Drugs:Amiodarone, Antibiotics (dapsone, isoniazid, metronidazole( AntiretroviralsChemotherapy(cisplatin, vincristine(, Phenytoin
    * 3-Toxins:Alcohol,Nitrous oxide Rarely: lead, arsenic, mercury, organophosphates, solvents
    * 4-Vitamin deficiencies:Thiamin, Pyridoxine, Vitamin B12, Vitamin E
    * 5-Infections: HIV, Leprosy, Brucellosis
    * 6-Inflammatory:Guillain–Barré syndrome, Vasculitis (polyarteritis nodosa, Wegener’s granulomatosis), rheumatoid arthritis, systemic lupus erythematous) Paraneoplastic
    * 7-Systemic medical conditions:Diabetes, Renal failure, Sarcoidosis
    * 8-Malignant disease: Infiltration
    * 9-Others:Paraproteinaemias, Amyloidosis

Myasthenia Graves

  • Def: Its progressive neuromuscular junction disorder due to ( effect on receptor). Autoimmune: IgG 80% 1Female>Male. *(20-40yrs) mainly affect two age group 15- 50yrs & >60yrs 2+ve F/h/ HLAB8 B/Thymic Abnormality: ASMA 15% Prognosis: Recovery in 3-6 months - Thymoma- Thymic hyperplasia.
    • Drug Induced 5% (Transient): D-pencilamine C/P: Muscle weakness characteristic: at end of day.After repeated ms work exercise R & R Course. Use of some drugs (Aminoglycosides, Ciprofloxacin, Propranolol & Quinine). Muscle affects: 1/Extralocular ms + Levetor palpebral superiors ms Diplopia & Ptosis. 2/Bulbar ms Dysphagia. *(Aspiration Pneumonia) 3/Shoulder Gridle proximal ms weakness of UL (weakness of combing hair). 4/Pelvic Gridle weakness on climbing stairs & arising from sitting position.
    • Trunk. 6/Respiratory ms RFII N.B: there is no sensory loss & complaining of Ms pain. Inv: 1/Edrophonium test: (Tension test) short acting. Improve symptoms within 30sec (best test). 2/EMG: decremental response. 3/Ab: Anticholine receptor Ab (80%) =Screening for other autoimmune.
      Treatment: 1/Pyridostigmine (Long Acting Anticholinesterase) DOC. 2 Thymoma +ve CT or CXR ve Ab Autoimmune Resection =Thymectomy.(60% improvement) Steroid. 3/Immunoglobulin. 4/Plasmaphresis or exchange. life threating due to respiratory failure type II, sudden Rapid progressive weakness especially respiratory ms. Severe dyspnea Treated by Emergency Intubation & Mechanical ventilation + plasma