Summary: Neurology

Table of Contents
1. Electroencephalography (EEG)
2. Lesion Localization
3. Headache
4. Migraine
5. Migraine Variants and Related Headaches
6. Epilepsy
7. Treatment of GCSE and AES Guidelines
8. Seizure Types and Features
9. Rare Epilepsy Syndromes
10. Parkinsonism
11. Key MRI/MRS Imaging Signs
12. Stroke
13. Stroke Syndromes by Vascular Territory
14. Lacunar Infarct Syndromes and Other Focal Signs
15. Ischemic Stroke Etiology and Risk Conditions
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Electroencephalography (EEG)

• EEG electrode labels: even = right, odd = left, Z = midline.
• Montage shows time (x-axis) and electrical activity (y-axis) from frontal, central, temporal leads.
• Provocative maneuvers: photic stimulation, hyperventilation, sleep deprivation/induction to elicit abnormalities.
• Artifacts: eye movements show in frontal leads, jaw clench in temporal leads; epileptic discharges usually involve multiple leads.
• Alpha coma: persistent unresponsive alpha rhythm seen in severe diffuse or brainstem injuries.

Lesion Localization

• Localizing signs relate to affected cortical or brainstem regions and cranial nerves (CN).

Headache

• Primary headaches: Tension-type (commonest), Migraine, Cluster, Idiopathic, Exertional.
• Secondary headaches: systemic infection, head injury, vascular disorders (stroke/aneurysm/AVM), subarachnoid hemorrhage, brain tumor; infections are the commonest secondary cause.

Migraine

• Migraine features: recurrent attacks (4-72 hours), pulsatile pain, nausea/vomiting, photophobia, phonophobia, worsened by physical activity; usually normal exam and no alternative cause.
• Migraine with aura: more common in females; aura includes visual symptoms (photopsia, scotomas).
• Pathophysiology notes: serotonin causes intracranial vasoconstriction with extracranial vasodilation stretching the dura mater producing pain; newer concepts involve CGRP-mediated vasodilation and cortical spreading depression.
• Abortive treatment: NSAIDs for mild-moderate attacks; triptans for moderate-severe or NSAID-refractory attacks (rizatriptan faster than sumatriptan; rizatriptan and eletriptan highly effective); IV prochlorperazine or dihydroergotamine for severe attacks.
• Prophylaxis: propranolol, flunarizine, gabapentin, pregabalin, amitriptyline.

Migraine Variants and Related Headaches

• Cluster headache: severe unilateral retro-orbital pain, strict periodicity (daily attacks during bouts), 1-2 short attacks daily; autonomic signs (epiphora, nasal congestion, red eye); attacks <3>
• Treatment: acute high-flow oxygen (12 L/min) and subcutaneous sumatriptan; adjunct gabapentin/pregabalin. Prophylaxis: verapamil, greater occipital nerve block.
• SUNCT: short unilateral neuralgiform attacks with conjunctival injection and tearing.
• Basilar migraine: brainstem aura symptoms (dizziness, vertigo) before headache.
• Ophthalmoplegic migraine: throbbing headache followed by ipsilateral III (±IV, V) nerve weakness with ptosis and possible diplopia.
• Familial hemiplegic migraine: calcium channel defect, family history, transient hemiparesis lasting days.
• Thunderclap headache raises concern for subarachnoid hemorrhage; acute retro-orbital pain with pupil changes suggests angle-closure glaucoma.

Epilepsy

• Epilepsy = long-term tendency to have ≥2 unprovoked seizures; caused by sudden neuronal hyperactivity with excitatory transmitters (aspartate, glutamate).
• Preferred antiepileptic drugs in pregnancy: lamotrigine, carbamazepine; topiramate and valproate are listed (valproate has concerns); phenobarbitone is less safe.
• Surgery is indicated for drug-resistant focal epilepsy.
• Status epilepticus: continuous seizure >30 minutes or repeated seizures without recovery; generalised convulsive status epilepticus (GCSE) often defined as convulsions >5 minutes.

Treatment of GCSE and AES Guidelines

• Initial (stabilisation, 0-5 min): airway, breathing, circulation, monitoring.
• Initial therapy (5-20 min): benzodiazepine-IM midazolam, IV lorazepam, or IV diazepam.
• Second therapy (20-40 min): IV fosphenytoin, IV valproate, or IV levetiracetam; if unavailable, IV phenobarbital.
• Third therapy (≥40 min): refractory status-repeat second-line or give anaesthetic doses (thiopental, midazolam, pentobarbital, propofol) with continuous EEG.
• First-line acute agents for GCSE: lorazepam or clonazepam; if ineffective consider phenytoin, valproate, levetiracetam; refractory-IV midazolam and/or propofol.

Seizure Types and Features

• Generalised tonic-clonic seizures: premonitory symptoms hours before; tonic phase 10-30 s, clonic phase 1-5 min with limb jerking, tongue bite, possible incontinence; post-ictal phase prolonged confusion/unconsciousness.
• Absence seizures: brief staring episodes in young children, preserved muscle tone, no post-ictal deficit, EEG 3 Hz spike-and-wave; triggered by hyperventilation/photosensitivity.
• Myoclonic seizures: sudden brief muscle jerks, age 10-19, morning predominance, EEG poly-spike 4-6 Hz.
• Focal seizures: arise from specific cortex-motor (precentral gyrus, may produce Jacksonian march and postictal Todd's palsy), sensory (postcentral tingling), versive (frontal eye deviation), visual (occipital hallucinations), psychomotor (temporal lobe automatisms).
• Associated ictal phenomena: déjà vu, jamais vu, complex multimodal hallucinations, automatisms.
• Post-seizure serum prolactin rises.

Rare Epilepsy Syndromes

• Mesial temporal lobe epilepsy (MTLE): history of atypical febrile seizures and family epilepsy; focal seizures with automatisms; EEG shows anterior temporal spikes; MRI may show hippocampal sclerosis; often drug-resistant but may respond to surgery.
• Lennox-Gastaut syndrome: multiple seizure types (tonic-clonic, atonic, atypical absence), slow (≈2.5 Hz) spike-and-wave on EEG, frequent cognitive impairment; linked to diffuse CNS injury or maldevelopment.
• Juvenile myoclonic epilepsy (JME): adolescent-onset generalized myoclonic jerks (morning), triggered by sleep deprivation; often coexists with GTCS and sometimes absence seizures; generally responsive to anticonvulsants.
• Lafora disease (progressive myoclonic epilepsy): myoclonus and GTCS, occipital visual hallucinations, progressive degeneration (cognitive/behavioral decline, dysarthria, ataxia, later spasticity and dementia); early EEG slowing and photosensitivity; PAS-positive Lafora bodies on skin biopsy; MRI often normal early.
• Unverricht-Lundborg disease: onset 6-16 years with stimulus-sensitive myoclonus and tonic-clonic seizures.

Parkinsonism

• Parkinson's disease (PD): second commonest neurodegenerative disorder after Alzheimer's; pathology: loss of dopaminergic neurons in the substantia nigra pars compacta, reduced striatal dopamine, and Lewy bodies.
• Clinical diagnosis: tremor, rigidity, bradykinesia historically; resting tremor, asymmetry, and marked levodopa responsiveness are reliable features; anosmia may precede motor signs by years.
• Causes: idiopathic/sporadic (common), genetic forms; secondary parkinsonism from drugs (antipsychotics), tumors, infections, toxins (manganese, CO, carbon disulfide), liver failure, normal pressure hydrocephalus; atypical parkinsonism: multiple system atrophy, progressive supranuclear gaze palsy, corticobasal degeneration.
• Investigations: PET/SPECT show reduced striatal dopaminergic uptake (mainly posterior putamen); imaging reserved for complex cases.
• Treatment: levodopa with a peripheral decarboxylase inhibitor (reduces peripheral side effects); initial dopaminergic side effects include nausea, vomiting, orthostatic hypotension-dose adjustment often helps.
• Other drugs: non-ergot dopamine agonists (pramipexole, ropinirole, rotigotine); rotigotine available as daily patch; apomorphine injectable rescue for severe off episodes; MAO-B inhibitors (selegiline, rasagiline) reduce dopamine breakdown; COMT inhibitors prolong levodopa effect and reduce off time.
• Surgery: deep brain stimulation (DBS) targeting STN or GPi improves off time and dyskinesias but does not help levodopa-unresponsive or non-dopaminergic features (freezing, falls, dementia).

Key MRI/MRS Imaging Signs

• Tigroid appearance on MRS: Pelizaeus-Merzbacher disease.
• "Face of panda": Wilson's disease.
• "Eye of tiger": pantothenate kinase-associated neurodegeneration.
• "Hot cross bun": multiple system atrophy.
• "Hummingbird sign": progressive supranuclear gaze palsy.

Stroke

• Stroke: sudden focal neurological deficit of vascular cause lasting >24 hours. TIA resolves within 24 hours. RIND (minor stroke) resolves within 72 hours.
• Risk after TIA assessed by the ABCD2 score (clinical tool).

Stroke Syndromes by Vascular Territory

• ACA: contralateral leg-predominant weakness/sensory loss; bladder control loss from hypertonic detrusor.
• MCA superior division: contralateral face/arm weakness, Broca's aphasia; inferior division: visual field defects (contralateral inferior quadrantanopia), sensory deficits, Wernicke's aphasia, neglect.
• Internal carotid: transient monocular blindness (amaurosis fugax).
• PCA: Parinaud syndrome, Claude's, Weber's features (third nerve palsy variants), cortical blindness or prosopagnosia with P1 occlusion; cortical blindness shows preserved pupillary reflex and Anton syndrome (denial of blindness).
• Basilar: brainstem syndromes (e.g., Millard-Gubler: ipsilateral VI/VII palsy with contralateral hemiplegia); most strokes are ischaemic (≈2/3) versus hemorrhagic (≈1/3).
• PICA (Wallenberg/lateral medullary): ipsilateral ataxia, ipsilateral facial sensory loss, ipsilateral Horner's syndrome, contralateral limb pain/temp loss, nystagmus/vertigo, dysphagia/dysarthria, hiccups.

Lacunar Infarct Syndromes and Other Focal Signs

• Pure motor hemiparesis: common lacunar syndrome (internal capsule, corona radiata, pons) - face, arm, leg equally affected without cortical signs.
• Pure sensory stroke: typically thalamic - contralateral sensory loss across modalities, with dysesthesias.
• Anterior choroidal artery syndrome: contralateral hemiplegia, hemianesthesia, homonymous hemianopia (may be partial due to collateral supply).
• Balint syndrome: parieto-occipital damage causing simultanagnosia, oculomotor apraxia, optic ataxia (seen after severe hypoxia/CPR).
• Ocular bobbing: bilateral pontine lesions (rapid down, slow up). Ocular dipping: diffuse anoxic damage (slow down, fast up).

Ischemic Stroke Etiology and Risk Conditions

• Thrombosis: gradual onset, often preceded by TIAs.
• Embolic stroke: sudden maximal deficit at onset, often cardiac source, higher seizure risk.
• Conditions increasing cerebral ischemia risk:
  • Vascular: atherosclerosis, vasculitis (eg SLE), infections (syphilis, HIV), artery dissection, drug abuse (cocaine, amphetamines, heroin), migraines, venous sinus thrombosis, chronic hypertension causing lacunar infarcts.
  • Cardiac: mural thrombus, rheumatic disease, arrhythmias, endocarditis, mitral valve prolapse, prosthetic valves.
  • Hematologic: thrombocytosis, polycythemia, sickle cell disease, leukocytosis, hypercoagulable states.