Detailed clinical learning notes for a medical student on the following topics Stroke Epilepsy Coma Epilepsy Headache Parkinson's Disease

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Clinical Learning Notes for Medical Students

Neurology: Core Topics

1. STROKE

Definition

Stroke is a clinical syndrome defined as the rapid onset of focal (or global) neurological deficit lasting >24 hours, caused by a vascular mechanism. A transient ischemic attack (TIA) is a similar episode lasting <24 hours (classically <1 hour), but over half of TIAs now show evidence of infarction on MRI, placing TIA and stroke on a continuum.

Fuster and Hurst's The Heart, 15th Edition, p. 805

Epidemiology

5th leading cause of death in the US; #1 cause of adult disability
~800,000 new/recurrent strokes per year in the US; one every 40 seconds
75% occur in individuals >75 years old
Ischemic: 87% | Intracerebral hemorrhage: 10% | Subarachnoid hemorrhage: 3%
Bradley and Daroff's Neurology in Clinical Practice

Classification (TOAST Criteria)

The TOAST classification (Trial of Org 10172 in Acute Stroke Treatment) is the most used mechanistic classification:

Subtype	Key Features
Large artery atherosclerosis	Stenosis/occlusion of major cerebral artery; cortical signs
Cardioembolism	AF, valvular disease, intracardiac thrombus; abrupt onset, peak deficit at onset
Small vessel occlusion (lacunar)	Deep white matter; classic lacunar syndromes (pure motor, pure sensory)
Other determined etiology	Hypercoagulable states, dissection, vasculitis
Undetermined	Cryptogenic; includes ESUS (embolic stroke of undetermined source)

Cardioembolism accounts for >40% of strokes in people >60 years - key causes: atrial fibrillation (AF is the most common), intracardiac thrombus post-MI, valvular disease.

Risk Factors

Modifiable: Hypertension (most important), diabetes, hyperlipidemia, smoking, AF, obesity
Non-modifiable: Age, sex (males >50; females >75), family history, ethnicity

Pathophysiology

Ischemic Stroke

Occlusion of a cerebral artery causes a central infarct core (irreversibly damaged) surrounded by a penumbra (ischemic but salvageable tissue)
Neurons begin dying within minutes of ischemia (energy failure → glutamate excitotoxicity → Ca²⁺ influx → cell death)
The penumbra is the therapeutic target

Hemorrhagic Stroke

Intracerebral hemorrhage (ICH): Most from hypertensive lipohyalinosis of small penetrating arteries (basal ganglia, internal capsule, thalamus, pons, cerebellum). Also: amyloid angiopathy (lobar), AVM, coagulopathy
Subarachnoid hemorrhage (SAH): Usually from ruptured berry aneurysm - presents as "thunderclap" headache ("worst headache of my life"), meningism, altered consciousness

Clinical Syndromes

Artery	Key Clinical Features
MCA	Contralateral hemiplegia (arm > leg), hemisensory loss, homonymous hemianopia; aphasia (dominant hemisphere) or neglect (non-dominant)
ACA	Contralateral leg > arm weakness; abulia, urinary incontinence
PCA	Homonymous hemianopia (with macular sparing), visual agnosia, memory deficits
Posterior circulation (PICA/AICA/basilar)	Vertigo, ataxia, diplopia, dysphagia, Horner's syndrome, crossed deficits
Lacunar (internal capsule)	Pure motor hemiplegia, pure sensory stroke, ataxic hemiparesis, dysarthria-clumsy hand

Acute Management

Investigations

CT head (non-contrast): First line - excludes hemorrhage (bright = bleed)
CT angiography/MR angiography: Detects large vessel occlusion (LVO)
MRI DWI: Most sensitive for early ischemia
ECG, cardiac monitoring: AF detection
Bloods: FBC, coagulation, glucose, lipids

Treatment

1. IV Thrombolysis (rtPA/alteplase)

Indication: Ischemic stroke, symptom onset ≤4.5 hours, no contraindications
Dose: 0.9 mg/kg IV (max 90 mg); 10% as bolus, remainder over 60 min
Contraindications include: anticoagulant use with elevated INR, major surgery <14 days, rapidly improving symptoms, previous ICH, BP >185/110 (must be treated first)

2. Endovascular Thrombectomy (EVT)

Indication: LVO (typically MCA/ICA), within 6-24 hours in selected patients with salvageable penumbra (DAWN/DEFUSE-3 criteria)
Dramatically improves outcomes in LVO - NNT ≈ 2-3 to improve by ≥1 mRS point

3. Blood Pressure Management

Pre-thrombolysis: Target <185/110 mmHg
Post-thrombolysis: Maintain <180/105 mmHg for 24h
ICH: Target SBP <140 mmHg

4. Antiplatelet Therapy

Aspirin 300 mg within 24h (only if hemorrhage excluded and tPA not given)
Dual antiplatelet (aspirin + clopidogrel) for 21 days in TIA or minor ischemic stroke (POINT/CHANCE trials)

Secondary Prevention

Mechanism	Treatment
Large artery atherosclerosis	Antiplatelet + statin + carotid endarterectomy/stenting if carotid stenosis >70%
Cardioembolism (AF)	Anticoagulation (DOACs preferred over warfarin)
Lacunar/small vessel	Antiplatelet + intensive BP control

Lifestyle: BP control, smoking cessation, diabetes management, exercise

Complications Post-Stroke

Dysphagia (28-65%): Screen before oral feeding; risk of aspiration pneumonia
DVT/PE: TEDS, early mobilization, LMWH
Seizures: Occur in ~4-8% acutely
Depression: Common - affects recovery
Spasticity, shoulder pain, contractures

2. EPILEPSY

Definition

Epilepsy is a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures. A single unprovoked seizure does not constitute epilepsy. Diagnosis requires:

≥2 unprovoked seizures >24 hours apart, OR
1 unprovoked seizure with ≥60% risk of recurrence, OR
Diagnosis of an epilepsy syndrome

A seizure is a transient occurrence of signs/symptoms due to abnormal excessive or synchronous neuronal activity.

Classification (ILAE 2017)

The most recent ILAE revision classifies seizures as:

A. By Onset

Category	Description
Focal onset	Originates within networks limited to one hemisphere
Generalized onset	Rapidly engages bilaterally distributed networks from onset
Unknown onset	Insufficient information to classify

B. Focal Seizures (replaced "partial")

Focal aware seizure (FAS) = old "simple partial" - awareness preserved throughout
- Auras are a form of FAS (purely subjective experience)
Focal impaired awareness seizure (FIAS) = old "complex partial" - any alteration in awareness
Focal to bilateral tonic-clonic (FBTC) = old "secondarily generalized"

C. Generalized Seizures

Type	Clinical Features
Absence	Brief (5-10s) staring spells; abrupt onset/offset; 3 Hz spike-wave on EEG; no postictal confusion; typical in childhood
Myoclonic	Brief, sudden muscle jerks; often in mornings; key in juvenile myoclonic epilepsy (JME)
Tonic-clonic (GTC)	Tonic phase (stiffening, epileptic cry, cyanosis) → clonic phase (rhythmic jerking) → postictal confusion and sleep; tongue biting, incontinence common
Tonic	Sustained muscle contraction, often during sleep
Atonic (drop attacks)	Sudden loss of muscle tone; risk of falls/injury
Clonic	Rhythmic jerking without prior tonic phase

EEG in Epilepsy

Epileptiform activity (spikes and sharp waves) is the hallmark - found in ~90% of patients with epilepsy
Only ~2% of people without epilepsy have epileptiform discharges
A normal interictal EEG does not exclude epilepsy
Video-EEG monitoring during a typical attack is the gold standard for diagnosis
Photoparoxysmal response: Spike-wave bursts elicited by photic stimulation - seen in photosensitive epilepsies

Key Epilepsy Syndromes

Syndrome	Age	EEG	Key Features	Treatment
Childhood absence epilepsy	4-12 yr	3 Hz spike-wave	Frequent absences; usually remits in adolescence	Ethosuximide, valproate
Juvenile myoclonic epilepsy (JME)	Adolescence	Polyspike-wave	Morning myoclonus, GTC, photosensitivity; lifelong	Valproate (drug of choice)
Temporal lobe epilepsy	Any	Temporal sharp waves	FIAS with automatisms; most common adult focal epilepsy	Carbamazepine/oxcarbazepine
West syndrome (infantile spasms)	<1 yr	Hypsarrhythmia	Flexion spasms; developmental regression	ACTH, vigabatrin
Lennox-Gastaut syndrome	2-8 yr	Slow spike-wave	Multiple seizure types; cognitive impairment	Valproate, lamotrigine, clobazam

Anti-Epileptic Drugs (AEDs)

Drug	Mechanism	Key Uses	Major Side Effects
Sodium valproate	Na⁺ channel + GABA	Broad-spectrum (GTC, absence, myoclonic)	Teratogenic, weight gain, hepatotoxicity, thrombocytopenia
Carbamazepine	Na⁺ channel	Focal seizures	Diplopia, ataxia, hyponatremia, rash (SJS risk with HLA-B*1502)
Lamotrigine	Na⁺ channel	Focal + generalized	Rash (SJS), slow titration needed; safe in pregnancy
Levetiracetam	SV2A binding	Broad spectrum; add-on	Behavioral side effects (irritability, depression)
Ethosuximide	T-type Ca²⁺ channel	Absence only	GI side effects
Phenytoin	Na⁺ channel	Status epilepticus, focal	Zero-order kinetics, gum hypertrophy, ataxia, cerebellar atrophy
Clobazam	GABA-A	Add-on	Sedation
Topiramate	Na⁺ + GABA + AMPA	Focal + generalized	Cognitive impairment ("Dopamax"), weight loss, nephrolithiasis

Teratogenicity: Valproate has the highest risk of neural tube defects and neurodevelopmental harm - avoid in women of childbearing age where possible.

Status Epilepticus

Definition: Seizure lasting >5 minutes OR ≥2 seizures without recovery of consciousness
Emergency - neuronal injury begins after 30 minutes
Management (ABCDE + stepwise):
1. Lorazepam 0.1 mg/kg IV (or midazolam IM if no IV access)
2. Levetiracetam 60 mg/kg IV, or phenytoin 20 mg/kg IV, or valproate 40 mg/kg IV
3. Phenobarbital 15-20 mg/kg IV
4. RSI + propofol/midazolam/thiopentone (refractory SE - ITU)

3. COMA

Definition and Levels of Consciousness

Coma is a state in which the patient is incapable of being aroused by external stimuli or inner need - eyes closed, unresponsive. Levels of altered consciousness exist on a spectrum:

Level	Description
Alert	Normal wakefulness
Drowsiness/Obtundation	Reduced alertness; arousable to verbal stimuli
Stupor	Only aroused by vigorous, repeated stimulation; returns to unresponsiveness when stimulus removed
Coma	Completely unarousable; eyes closed; no purposeful responses

Adams and Victor's Principles of Neurology, 12th Edition

Pathophysiology

Consciousness requires the ARAS (ascending reticular activating system) in the brainstem to be intact, plus functioning bilateral cerebral cortices. Coma results from:

Bilateral cortical dysfunction (e.g., metabolic, hypoxia, bilateral strokes)
Brainstem (ARAS) dysfunction (e.g., brainstem hemorrhage, herniation)
A single hemispheric lesion alone should NOT cause coma unless it causes mass effect and herniation

Herniation syndromes:

Uncal herniation: Medial temporal lobe compresses midbrain → ipsilateral blown pupil (CN III compression), contralateral hemiparesis → then bilateral signs
Central herniation: Rostrocaudal deterioration → Cheyne-Stokes breathing → decorticate → decerebrate posturing → respiratory failure

Causes of Coma - Mnemonic: AEIOU TIPS

Letter	Causes
A	Alcohol, Acidosis
E	Epilepsy, Electrolytes
I	Insulin (hypoglycemia), Intoxication
O	Overdose (drugs/toxins), Oxygen (hypoxia)
U	Uraemia
T	Trauma, Temperature (hypo/hyperthermia)
I	Infection (meningitis, encephalitis, sepsis)
P	Psychiatric (rare), Poisoning
S	Stroke, Structural lesion, SAH

Glasgow Coma Scale (GCS)

Component	Response	Score
Eye Opening (E)	Spontaneous	4
	To voice	3
	To pain	2
	None	1
Verbal (V)	Oriented	5
	Confused	4
	Inappropriate words	3
	Incomprehensible sounds	2
	None	1
Motor (M)	Obeys commands	6
	Localizes pain	5
	Withdraws to pain	4
	Abnormal flexion (decorticate)	3
	Extension (decerebrate)	2
	None	1

GCS ≤8 = Coma (protect airway - consider intubation)
GCS 9-12 = Moderate impairment
GCS 13-15 = Minor impairment
Total score: 3 (minimum) to 15 (normal)

FOUR Score: Alternative scale that adds brainstem reflexes and respiratory pattern - useful in intubated patients (where verbal score cannot be assessed).

Tintinalli's Emergency Medicine

Special States Related to Coma

State	Key Features
Vegetative State (Unresponsive Wakefulness)	Wake-sleep cycles present, eyes open spontaneously; no awareness, no purposeful response; can swallow, grimace, groan
Minimally Conscious State (MCS)	Some evidence of awareness (follows commands inconsistently, visual tracking, purposeful movements)
Locked-in Syndrome	Fully conscious but completely paralysed (basilar artery occlusion/pontine stroke); can communicate only via vertical eye movements
Brain Death	Irreversible cessation of all brain including brainstem function; no response, no brainstem reflexes, apnoea test positive
Akinetic Mutism	Alert-appearing but with no movement or speech; bifrontal or cingulate lesions

Assessment of the Comatose Patient

Airway, Breathing, Circulation - immediate priority
Check glucose (Dextrostix) - give IV dextrose if hypoglycaemia
Give thiamine (100mg IV) before glucose in any malnourished/alcohol patient (prevents Wernicke's)
Naloxone if opiate overdose suspected
History from witnesses/relatives - speed of onset, preceding events, medications, PMHx
Neurological examination:
- Pupils (size, reactivity, symmetry)
- Eye movements (doll's eye, caloric testing)
- Corneal reflex
- Motor responses (posturing)
- Breathing pattern

Pupillary findings:

Unilateral dilated/fixed: CN III palsy (uncal herniation, PCA aneurysm)
Bilateral pinpoint: Pontine lesion OR opiate toxicity
Bilateral fixed dilated: Midbrain herniation OR atropine/sympathomimetic overdose
Bilateral small reactive: Metabolic/toxic coma (good prognostic sign)

Emergency Investigations

CT head (exclude haemorrhage, herniation)
Bloods: glucose, Na, K, Ca, urea, creatinine, LFTs, TFTs, full blood count, ABG, ammonia
Toxicology screen
Blood cultures, LP (if meningitis suspected and CT clear)
EEG (non-convulsive status epilepticus)

4. HEADACHE

Classification (ICHD-3)

Headaches are classified as:

Primary: The headache IS the disorder (migraine, tension-type, cluster, TACs)
Secondary: Headache is a symptom of another condition (SAH, meningitis, raised ICP, mass lesion)

Always exclude secondary ("dangerous") causes first

Red Flags ("SNOOPS4")

Letter	Feature
S	Systemic symptoms (fever, weight loss, immunosuppression)
N	Neurological deficit
O	Onset sudden (thunderclap) - SAH until proven otherwise
O	Older age, new onset headache >50 yrs (temporal arteritis, malignancy)
P	Previous headache history - change in pattern
P	Positional (worse lying down = raised ICP; better lying down = low-pressure headache)
P	Papilloedema
P	Progressive worsening

Any of these warrant urgent investigation (CT ± LP ± MRI).

Bradley and Daroff's Neurology in Clinical Practice

Migraine

Epidemiology

Prevalence ~15% population; 3:1 female predominance
Peak in reproductive years (20-40)

Diagnostic Criteria (ICHD-3)

At least 5 attacks lasting 4-72 hours with ≥2 of:

Unilateral location
Pulsating quality
Moderate-severe intensity
Aggravated by routine physical activity

Plus ≥1 of:

Nausea/vomiting
Photophobia + phonophobia

Migraine with aura: Reversible focal neurological symptoms (usually visual - scintillating scotoma, fortification spectra) lasting 20-60 min before headache onset. Visual aura is most common. Motor aura = hemiplegic migraine (rare).

Pathophysiology

Cortical spreading depression (CSD): A wave of neuronal depolarisation spreading at 3-5 mm/min - underlies the aura
Trigeminovascular activation: CSD and other mechanisms activate the trigeminal ganglion → release of CGRP, substance P, VIP → neurogenic inflammation of meningeal vessels → headache
CGRP plays a central role - basis for new drug classes (gepants, CGRP monoclonal antibodies)
The migraine brain is hyperexcitable, with reduced cortical habituation to stimuli

Treatment

Acute:

Drug	Dose	Notes
Simple analgesia (aspirin, ibuprofen, paracetamol)	Standard	First line mild-moderate
Triptans (5-HT1B/1D agonists)	e.g., Sumatriptan 50-100mg oral	Gold standard for moderate-severe; cause vasoconstriction + block CGRP release; avoid in CVD, hemiplegic migraine
Antiemetics (metoclopramide, prochlorperazine)	-	Aid absorption + direct benefit
Gepants (ubrogepant, rimegepant)	-	CGRP receptor antagonists; no vasoconstriction risk

Prophylaxis (indicated if ≥4 attacks/month, or ≥2 with disability):

Drug	Notes
Propranolol	First line; avoid in asthma, depression
Topiramate	Effective; teratogenic (folic acid antagonist); cognitive side effects
Amitriptyline	Useful if comorbid depression/insomnia
Valproate	Effective; teratogenic - avoid in women of childbearing potential
CGRP monoclonal antibodies (erenumab, fremanezumab, galcanezumab)	SC injection monthly; very effective, well-tolerated; newer agents

Tension-Type Headache (TTH)

Most common headache type
Bilateral, pressing/tightening (non-pulsating), mild-moderate severity
No nausea/vomiting; phonophobia OR photophobia (not both)
Not aggravated by routine activity
Usually lasts 30 min to 7 days
Treatment: Simple analgesia (paracetamol, ibuprofen); prophylaxis with amitriptyline if chronic (≥15 days/month)

Cluster Headache

Strictly unilateral, periorbital/temporal, severe/excruciating pain
Lasts 15-180 minutes (1-8 attacks/day)
Ipsilateral autonomic features: lacrimation, nasal congestion/rhinorrhoea, Horner's syndrome, ptosis, eyelid oedema
Restlessness (cannot lie still - opposite of migraine)
Occurs in "clusters" (weeks-months) with pain-free periods
Male predominance (5:1); nocturnal attacks common
Acute: 100% O₂ (12-15 L/min, 15 min) + subcutaneous sumatriptan
Prevention: Verapamil (first line), lithium, short-course corticosteroids (to break a cluster)

Medication Overuse Headache (MOH)

Occurs with use of analgesics/triptans >10-15 days/month for >3 months
Results in transformed (chronic daily) headache
Treatment: Withdraw the overused medication (expect worsening for 1-2 weeks) + bridge therapy

5. PARKINSON'S DISEASE

Definition

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterised by the triad of resting tremor, rigidity, and bradykinesia, with postural instability developing later. Pathologically defined by loss of dopaminergic neurons in the substantia nigra pars compacta and Lewy body (alpha-synuclein aggregate) formation.

Epidemiology

2nd most common neurodegenerative disorder (after Alzheimer's)
Prevalence ~1% >60 years; 3% >80 years
Slightly more common in males
Mean age of onset ~60-65 years; early-onset <50 years

Pathophysiology

Key pathological changes:

Loss of dopaminergic neurons in the substantia nigra pars compacta (SN pc) - symptoms appear when >60-80% of neurons are lost
Lewy bodies - eosinophilic intracytoplasmic inclusions containing misfolded alpha-synuclein protein
Braak staging: Pathology begins in olfactory bulb and dorsal vagal nucleus (Stage 1) → locus coeruleus (Stage 2) → SN (Stage 3-4) → neocortex (Stage 5-6)

Basal ganglia circuit disruption:

Normal: Dopamine from SN acts on striatum → facilitates desired movement via direct pathway + inhibits unwanted movement via indirect pathway
In PD: Dopamine loss → overactivation of subthalamic nucleus → increased inhibitory output from GPi to thalamus → reduced thalamocortical drive → bradykinesia

Clinical Features

Cardinal Motor Features (TRAP)

Feature	Description
Tremor	Resting tremor (3-6 Hz); "pill-rolling"; suppressed by movement; worse with stress
Rigidity	Lead pipe (uniform resistance throughout ROM) or cogwheel (ratchet-like, when tremor superimposed); affects axial muscles early
Akinesia/Bradykinesia	Slowness of movement initiation and execution; reduced amplitude of repetitive movements; hypomimia (masked face); micrographia; hypophonia
Postural instability	Late feature; loss of righting reflexes; festinating gait; falls

Classic gait: Stooped posture, reduced arm swing, short shuffling steps, festination (accelerating), difficulty initiating (freezing of gait), en bloc turning

Non-Motor Features (often precede motor symptoms)

Olfactory: Anosmia (may precede motor symptoms by years)
Sleep: REM sleep behaviour disorder (RBD) - important prodromal marker; excessive daytime sleepiness
Autonomic: Orthostatic hypotension, constipation, urinary dysfunction, excessive sweating
Neuropsychiatric: Depression (most common psychiatric comorbidity), anxiety, apathy, psychosis (hallucinations - typically visual, in later stages), dementia (Parkinson's disease dementia, PDD)
Cognitive: Mild cognitive impairment early; frank dementia in 30-50% (usually late)

Diagnosis

Diagnosis is clinical - based on UK Brain Bank criteria:

Step 1: Establish parkinsonism (bradykinesia + ≥1 of: rigidity, resting tremor, postural instability)
Step 2: Exclude alternative causes (stroke, neuroleptic use, repeated head trauma)
Step 3: Supportive features (3 or more):
- Unilateral onset
- Resting tremor
- Progressive disorder
- Asymmetry persisting
- Excellent response to levodopa (>70%)
- Levodopa-induced dyskinesia
- Clinical course ≥10 years

MRI: Usually normal - used to exclude vascular parkinsonism, PSP, MSA DaTscan (SPECT): Reduced dopamine transporter uptake in striatum - distinguishes PD from essential tremor (normal DaTscan) and drug-induced parkinsonism

Differential Diagnosis (Parkinson's Plus Syndromes)

Condition	Distinguishing Features	Levodopa Response
Progressive Supranuclear Palsy (PSP)	Vertical supranuclear gaze palsy, axial > limb rigidity, early falls, "hummingbird sign" on MRI, retrocollis	Poor
Multiple System Atrophy (MSA)	Early autonomic failure (OH), cerebellar features (MSA-C) or parkinsonism (MSA-P), "hot cross bun sign" in pons (MSA-C)	Initially partial, then fails
Corticobasal Degeneration (CBD)	Alien limb phenomenon, apraxia, cortical sensory loss, asymmetric akinetic-rigid syndrome	Poor
Dementia with Lewy Bodies (DLB)	Dementia precedes/concurrent with parkinsonism, fluctuating cognition, visual hallucinations, neuroleptic sensitivity	Variable
Drug-induced Parkinsonism	History of dopamine antagonist use (antipsychotics, metoclopramide); symmetric; normal DaTscan	Resolves on stopping drug
Vascular Parkinsonism	Lower-body predominant ("lower-half parkinsonism"), early falls, step-wise progression, white matter lesions on MRI	Poor
Essential Tremor	Postural/action tremor (not resting), bilateral, no bradykinesia/rigidity, normal DaTscan, family history	N/A

Pharmacological Treatment

Levodopa (L-dopa)

Most effective symptomatic treatment - gold standard
Always combined with carbidopa (or benserazide) - peripheral dopa-decarboxylase inhibitor that prevents peripheral conversion of levodopa to dopamine, reducing side effects (nausea, hypotension) and increasing CNS delivery
No evidence for delaying treatment

Motor complications (develop in up to 50% within 2-5 years):

Wearing off: Shortened duration of benefit; worse before next dose (end-of-dose akinesia)
Peak dose dyskinesia: Involuntary choreoathetoid movements when levodopa levels peak
On-off fluctuations: Unpredictable switching between responsive "on" and rigid/frozen "off" states
Management of fluctuations: Increase dose frequency, add COMT inhibitor (entacapone), add MAO-B inhibitor (selegiline, rasagiline), dopamine agonist, continuous duodenal infusion

Dopamine Agonists (Pramipexole, Ropinirole, Rotigotine patch)

Preferred as initial therapy in younger patients (<65 yrs, cognitively intact) to delay levodopa and reduce early motor complications
Less effective than levodopa
Side effects: Impulse control disorders (gambling, hypersexuality, binge eating - 1 in 6!), excessive daytime somnolence, leg oedema, hallucinations

MAO-B Inhibitors (Selegiline, Rasagiline, Safinamide)

Block breakdown of dopamine; mild symptomatic benefit; neuroprotective effect debated
Add-on therapy; reduce "wearing off"

COMT Inhibitors (Entacapone, Opicapone, Tolcapone)

Prevent peripheral breakdown of levodopa → smoother, more sustained plasma levels
Always used in combination with levodopa; reduce "wearing off" time

Anticholinergics (Trihexyphenidyl/Benzhexol, Benztropine)

Primarily for tremor in younger patients
Avoid in elderly (confusion, urinary retention, constipation, hallucinations)

Amantadine

Mild dopaminergic + anticholinergic effects
Uniquely effective for levodopa-induced dyskinesia

Non-Pharmacological Treatment

Deep Brain Stimulation (DBS): High-frequency stimulation of subthalamic nucleus (STN) or globus pallidus internus (GPi); reduces OFF time and dyskinesias; best for patients with good levodopa response but disabling motor complications
Physiotherapy: Gait re-training, balance, falls prevention
Speech therapy: Dysarthria, dysphagia, LSVT (Lee Silverman Voice Treatment)
Occupational therapy: Activities of daily living

Neuropsychiatric Features in PD

Feature	Details
Depression	Most common psychiatric disturbance; related to disruption of dopamine, noradrenaline, serotonin pathways; treat with SSRIs (first line) or TCAs
Psychosis/Hallucinations	Typically visual; occur in up to 40% (late); usually medication-induced; do NOT use typical antipsychotics (worsen parkinsonism); use quetiapine or clozapine (most effective) or pimavanserin
Cognitive impairment/Dementia	Progressive; rivastigmine (cholinesterase inhibitor) approved for PDD
Impulse control disorders	Linked to dopamine agonists; require dose reduction/cessation
REM sleep behaviour disorder	Patients act out dreams; may precede motor symptoms by years

Summary Comparison Table

Feature	PD	DLB
Motor before cognition	Yes (usually)	No - dementia concurrent or first
Hallucinations	Late, medication-induced	Core feature, early, not medication-induced
Neuroleptic sensitivity	Motor worsening only	Severe sensitivity - increased morbidity/mortality
Fluctuating consciousness	Only if delirious	Core feature

Bradley and Daroff's Neurology in Clinical Practice; Goldman-Cecil Medicine, 2025

Key Sources

Bradley and Daroff's Neurology in Clinical Practice (primary neurology reference throughout)
Fuster and Hurst's The Heart, 15th Edition (stroke - cardioembolic mechanisms, TOAST classification)
Adams and Victor's Principles of Neurology, 12th Edition (coma spectrum)
Plum and Posner's Diagnosis and Treatment of Stupor and Coma (coma, brain death)
Tintinalli's Emergency Medicine (GCS, coma management)
Goldman-Cecil Medicine, 22nd/2025 Edition (Parkinson's disease treatment)
Goodman & Gilman's Pharmacological Basis of Therapeutics (AED and PD pharmacology)These notes are drawn directly from the medical library, covering all 5 topics (Epilepsy listed once, as requested). Here is a quick guide to what is included:

What These Notes Cover

1. Stroke

Epidemiology (800,000/yr US; 87% ischemic)
TOAST classification (large artery, cardioembolic, lacunar, cryptogenic)
Vascular territory syndromes (MCA, ACA, PCA, lacunar, posterior fossa)
Acute management: IV tPA (≤4.5h), endovascular thrombectomy (LVO ≤24h), BP targets
Secondary prevention by mechanism, post-stroke complications

2. Epilepsy

ILAE 2017 seizure classification (focal aware/impaired awareness/to bilateral tonic-clonic; generalised types)
EEG interpretation: epileptiform discharges, photoparoxysmal response
Key syndromes: childhood absence, JME, temporal lobe epilepsy, West syndrome, Lennox-Gastaut
AED table: mechanism, indication, key side effects (including valproate teratogenicity)
Status epilepticus stepwise management

3. Coma

Spectrum of consciousness (drowsiness → stupor → coma)
Pathophysiology (ARAS + bilateral cortex; herniation syndromes)
AEIOU TIPS mnemonic for causes
Full GCS table (adult + paediatric scoring)
FOUR score; pupillary signs by lesion level
Vegetative state, MCS, locked-in syndrome, brain death - key distinctions
Emergency assessment and management approach

4. Headache

Red flag features (SNOOPS4) + imaging indications
Migraine: pathophysiology (CSD, trigeminovascular system, CGRP), ICHD-3 criteria, acute (triptans, gepants) and prophylactic treatment (propranolol, topiramate, CGRP mAbs)
Tension-type headache vs migraine
Cluster headache: autonomic features, acute O₂ + sumatriptan, verapamil prophylaxis
Medication overuse headache

5. Parkinson's Disease

TRAP motor features, Braak staging, alpha-synuclein/Lewy body pathology
Non-motor features (RBD, anosmia, depression, autonomic)
UK Brain Bank diagnostic criteria, DaTscan
Parkinson's Plus differentials (PSP, MSA, CBD, DLB) with distinguishing features
Levodopa pharmacology and motor complications (wearing off, dyskinesia)
Full drug table: levodopa/carbidopa, dopamine agonists, MAO-B inhibitors, COMT inhibitors, amantadine, anticholinergics
DBS indications; neuropsychiatric management

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