Neurology Mbchb4


Acute Confusional State

1. Definition – Acute confusional state
a. Global impairment of higher mental function
b. Due to bilateral dysfunction of both hemispheres
c. Acute or subacute usu developing over hours/days
d. Assoc with impaired orientation and drowsiness and often distorted perceptions of sensory info (illusions)
e. Impt to identify and tx underlying cause as this usu leads to resolution of confusion
2. Etiology – 3 main causes
a. Systemic or metabolic d/os (most common cause)
i. Ø a primary neurologic d/o and involvement of the brain may be more obvious than dis in the primary organ
ii. May be the first indication of an underlying systemic or metabolic d/o
iii. Most common cause in elderly and hospitalised pts
iv. May be due to a combination of factors – eg elderly pt w incipient dementia who is hospitalised w a UTI
v. CT/MRI Scans and CSF exam are all normal
vi. Specific causes
1. drugs – intoxication or withdrawal
2. acute systemic infection – esp children and elderly eg pneumonia, UTI
3. organ failure – eg uraemia, LF, HF, respiratory failure
4. hypoxia/hypercapnia
5. acid-base abnormalities (m.acidosis or alkalosis)
6. hyponatremia (hypernatremia)
7. hypercalcemia
8. hypo or hypermagnesemia
9. hypogly/hypergly
10. co-factor deficiency – thiamine (wernicke-korsakoff syndr), niacin (pellagra)
b. Acute bilateral cerebral hemisphere dis
i. Infections – eg meningitis or encephalitis
ii. Subarachnoid hemorrhage
iii. Multifocal cerebral ischemia – eg hyperviscosity, hypertensive encephalopathy, disseminated intravascular coagulopathy
iv. Head injury – diffuse injury, contusions
v. Epileptic seizures – post ictal state, ongoing minor seizures (minor status epilepticus)
vi. Migraine
c. Focal mass lesions, ↑ ICP and a shift in intracranial contents
i. Unilateral lesion in one cerebral hemisphere may cause dysfunction of the other by producing ↑ ICP and a shift of intracranial contents
ii. Infarction (with edema)
iii. Intracerebral hemorrhage
iv. Subdural hematoma (esp in older people, alcoholics)
v. Tumor
vi. Abscess
3. Clinical Features
a. Main feature = General reduction in all mental activity
b. Specific features
i. Drowsiness
ii. Inattentiveness
iii. Disorientation – time and place
iv. Illusions or reduced/distorted perception
v. Reduced speed and clarity of thinking
vi. Impaired memory
c. Examination
i. Assessment of cogv function
1. fluency and content of speech
2. Orientation
3. Mood/Affect
4. Memory
5. Mental activity
ii. Neurological exam
1. Papilledema (↑ ICP)
2. Focal neurological signs – visual fields, pupils/eye mvments, focal weakness
iii. General medical exam
1. Temperature
2. Evidence of systemic dis
3. Neck stiffness/meningism (infection/subarachnoid hem)
4. Delirium
a. Definition
i. Often used synonymously with acute confusional state but in neurology –
ii. Delirium is a form of confusional state with additional features of –
1. agitation (eg pulling tubes out etc)
2. tremulousness
3. autonomic overactivity
4. visual hallucinations
5. convulsions
iii. DTs (delirium tremens) is the classic form of delirium
iv. Untx, delirium has a mortality of 20%
b. Causes
i. Any of the conditions as per acute confusional state
ii. Drug intoxication – amphetamines, steroids (even 60 mg prednisone!), atropine
iii. *Withdrawal states – alcohol, sedative drugs (eg benzos)
iv. *Acute infections – esp children
v. Encephalitis
vi. Head injury
5. Differential Dx
a. Psychiatric d/o – esp psychosis, psychogenic d/o
b. Wernickes dysphasia
c. Dementia
i. Comes on over months/years
ii. Acute metabolic or systemic illness may precipitate an acute confusional state in a pt w a pre-existing but unrecognised dementia
iii. People with dementia aren’t drowsy or delirious
6. Confusional state in an alcoholic (or drug addict)
a. Acute intoxication
b. Alcohol withdrawal eg DTs
c. Post-ictal state following seizure
d. Head injury (falls or assault)
e. Wernickes encephalopathy (thiamine deficiency)
f. Systemic infection
7. Ixs
a. Search for systemic disturbance or brain dis with expectation that a potentially treatable cause will be found and the confusional state will resolve w appropriate tx
b. First line ixs
i. FBC, Na, calcium, Creatinine, LFTs, glucose
ii. ABGs – pH, PO2, PCO2
iii. Blood cultures, urine examination, urine drug screen
iv. CXR
c. 2nd line ixs
i. Mg2+, TFTs, adrenal screen
ii. Consider CT or MRI if there are focal signs or the pt is stuporose
iii. Consider CSF exmn if fever is present or if above lab tests negative
iv. Consider EEG if concerned about ongoing seizures
8. Management
a. Tx the underlying cause – consider stopping drugs that may cause confusional state
b. Etal interventions – prevent from injury, optimal stimulation
c. Avoid sedation if possible – use with caution if delirious/agitated but reqd if thrashing about etc, use only one drug, review dose daily
i. Haloperidol 0.5-1 mg po bd
ii. Benzodiazepine eg Clonazepam 1-2mg/day
d. Special situations
i. Hypoglycemia – 50 mls 50% dextrose
ii. Thiamine deficiency – always give thiamine before giving a glucose load if wernickes is a possibility

Stupor and Coma

1. Normal state of consciousness has 2 components
a. Alertness
i. Depends on the integrity of brain stem reticular activating sys which extends from the tegmentum of the midpoins to the diencephalons and acts upon both hemispheres
b. Content of conciousness
i. Sum of the thought processes or higher mental functions
ii. Depends on both hemispheres
c. In brain d/os, both components are often affected together, but depending on the nature of the dis processes and its site, involvement of one component may predominate
2. Drowsiness → Stupor → Coma
a. Impairment of consciousness ranges from drowsiness to coma as judged by a pt’s spontaneous activity and by their reaction to external stimuli
b. Stupor – sleep-like unresponsivenss from which the pt may be temporarily aroused by vigorous or repeated stimulation
c. Coma – pt cannot be roused, no response to external stimulation
d. Distinction betw the two is not well defined
3. Terminology
a. Tentorial notch – triangular opening in tentorium cerebelli through which the b/stem extends from the posterior into the middle cranial fossa
b. Tentorium – strong fold dura mater roofing over the posterior cranial fossa with an anterior median opening, the tentorial notch through which the midbrain passes

4. Etiology of coma
a. Structural
i. Infratentorial structural lesion (mass or destructive)
1. Lesion affects RAS in upper brain stem
a. Either directly by destroying the b/stem eg brainstem hemorrhage
b. Or by direct brain stem compression eg cerebellar tumor
2. ~15% of causes of coma
3. Most common cause – vascular (occlusion of vasilar artery or hem into pons or midbrain)
4. Mass in cerebellum may compress upper b/stem as it expands – eg cerebellar infarct, hemorrhage, tumor, abscess
5. Typical Hx
a. Sudden or subacute onset
b. Diplopia
c. Ataxia
d. Vertigo
e. N/V
f. Headache
6. Exmn findings – ‘brainstem signs’
a. Diplopia w a complex eye mvment d/o
b. Impaired reflex eye mvments
c. Abnormal papillary responses
d. Other CN lesions
ii. Supratentorial mass lesion
1. ~20% of causes of coma
2. Mass lesion in a cerebral hemisphere affects RAS indirectly as a result of displacement of brain subst from one component to another
3. Swollen brain herniates across the midline and down the tentorial notch (transtentorial herniation)
4. Upper b/stem is compressed and stretched w interruption of its blood supply from small branches of the basilar artery
5. Tentorial herniation may either be central or lateral, in which case the uncus of the medial temporal lobe herniates through the tentorial notch and frequently –
a. compresses CN3
b. the contralateral peduncle causing an ipsilateral hemiparesis (false localising sign)
c. posterior cerebral artery causing a homonymous hemianopia
6. Typical presentation
a. S/S of focal brain dis – eg headache, hemiparesis, aphasia, partial epilepsy etc
b. Focal neuro signs due to either primary lesion or a false localising sign
c. May be bilateral UMN signs eg Plantars ↑↑
d. Early signs of displacement and compression of upper brain stem incl reduced alertness anf freq yawning
e. Signs of ↑ ICP –
i. papilledema (often late sign)
ii. cushings sign - ↑ BP (+ relative bradycardia (late sign))
7. Causes of supratentorial mass lesion causing coma
a. Intracerebral hemorrhage
b. Large ischemic stroke w edema
c. Subdural or Extradural hematoma
d. Brain tumour
e. Brain abscess
8. Pointers to a supratentorial cause
a. Hx
i. Headaches
ii. Seizures
iii. Focal supratentorial sxs – dysphasia, hemiparesis, hemisensory loss
b. Exmn
i. Focal supratentorial signs – dysphasia, hemiparesis/hemisensory loss, hemianopia
ii. Focal b/stem signs – diplopia w complex eye mvment d/o, impaired reflex eye mvments, unequal pupils
b. Diffuse, multifocal or metabolic
i. Metabolic encephalopathy most common cause of coma ~65%
ii. Diffuse cerebral dysfunction affecting both RAS and central hemispheres → coma
iii. Metabolic – used in broadest sense to incl endogenous metabolic d/os (eg hypoxia), intoxications and diffuse intracranial d/os (eg meningitis)
iv. Causes
1. Deprivation of O2, substrate or metabolic co-factors
a. Hypoxia (↓ O2 in blood) – interference w O2 supply and normal cerebral blood flow
b. Ischemia (disrupted blood supply) – diffuse or multifocal interference w blood supply
c. Hypoglycaemia
d. Co-factor deficiency – thiamine, niacin
2. Organ disease (other than brain)
a. Non-endocrine organs – liver, kidney, lung, pancreatic failure
b. Endocrine organs – hypopituitarism, hypothyroidism
3. Exogenous poisons (incl drugs)
a. Sedatives – barbiturates, non-barbiturate hypnotics
b. Acid poisons
c. Other pschyotropic drugs
d. Others – anticholinergics, lithium, anticonvulsants
4. Electrolyte and acid-base abnormalities
a. Water and Na – hypo or hypernatremia
b. M.acidosis
c. Alkalosis
d. Hypo and hypermagnesemia
e. Hypercalcemia
5. Disorders of temperature regulation
6. Infections or inflammation of the brain
a. Encephalitis
b. Meningitis
7. Others
a. Post-epileptic seizure
b. Head injury
c. Subarachnoid hemorrhage
8. Note – in mild forms, these d/os often affect the content of conciousness more than the level of arousal and produce a confusional state w variable degrees of drowsiness; however, when severe, these d/os produce a stupor or coma
v. Pointers to diffuse, multifocal or metabolic coma
1. Hx
a. Gradual or progressive onset
b. Sudden onset suggests hemorrhage
c. Infections may have sudden or gradual onset
2. Exmn
a. Symmetrical neuro findings
b. Pupillary reactions usu retained (even if other b/stem ocular reflexes are lost eg doll’s eye or caloric testing)
c. Inf/hemorrhage causes fever and neck stiffness
d. Head injury – look for blood or CSF in ear or bruising behind ear
e. Signs of systemic dis
f. Abnormal breathing pattern
c. Distinguishing coma due to metabolic or structural causes – impt clinical points
i. Neurological signs are symmetrical w/o focal feats
ii. Pupillary responses to light are relatively resistant to metabolic causes of coma so typically retained even after b/stem reflexes (eg reflex eye mvments) are lost
iii. Breathing pattern often abnormal in metabolic coma
1. Hyperpnea (hyperventilation or kussmaul breathing) in m.acidosis (DKA, uremia, lactic acidosis) + central neurogenic hypervent
2. Hypovent occurs w some types of lung dis and w CNS respiratory depr
d. Traps
i. Some structural lesions give feats of metabolic encephalopathy/coma eg subarachnoid hem, acute hydrocephalus
ii. Some metabolic encephalopathy/coma can cause focal signs – eg hypoglycaemia
5. Differential Dx
a. Not every unresponsive pt is in a coma
b. Locked in syndrome
i. Appear to be unconscious but are in fact awake and alert but unable to respond
ii. Paralysis of arms, legs, facial, bulbar muscles – can not speak, move tongue or swallow
iii. Horizontal eye mvments are paralysed, but vertical eye mvments are preserved (main means of communication)
iv. Vision, hearing and somatosensory sensation are intact
v. Usu caused by a lesion in the basis pontis (ventral pons) which interrupts the corticospinal and corticobulbar pways, but spares the somatosensory pways and RAS
vi. Usual cause is an infarct caused by occlusion of the basilar artery or a vertebral art
c. Pschogenic unresponsiveness
i. Resembles metabolic coma
ii. Unresponsive to stimulation (incl pain)
iii. Neurological exmn normal
iv. Pupils reactive to light
v. Often resists eye opening
vi. Ice cold calorics induce nystagmus (normal response) and EEG is normal
6. Assessment of the comatose pt
a. ABCs
b. Determine LOC
c. Coma scale – eye opening, speech and mvment of limbs (see below for terminology)
i. Eyes open /4
ii. Best verbal response /5
iii. Best motor response /6
d. Determine cause of coma
i. Hx from witnesses
ii. Exmn
1. Respiratory pattern
a. Hypopnea – metabolic coma eg drug overdose
b. Hyperpnea
i. Central neurogenic hyperventilation
ii. M.acidosis – eg DKA, uremia, lactic acidosis
iii. R.alkalosis – in HF, septic shock
iv. Hypoxia
c. Irregular gasping respirations
i. Structural b/stem lesions
2. Pupillary light reactions
a. Normal pupils → metabolic coma
b. Unilateral dilated pupil → transtentorial herniation, compression of the occulomotor n at tentorial notch
c. Mid-position, fixed pupils → midbrain lesion
d. Pinpoint pupils → pontine lesion
3. Reflex eye mvments
iii. Look for –
1. Signs of head injury
2. Signs of ↑ ICP
3. focal neurological signs
4. Meningism
5. Needle marks from IV drug use
6. Systemic illness
7. Medic alert bracelet
7. GCS Terminology
a. Orientated – knows who they are, where they are, date and time, can sustain a conversation
b. Confused – may converse, but fails orientation questions, answers other questions w obvious errors
c. Inappropriate – cannot converse, exclaims, shouts, swears
d. Incomprehensible – moans or grunts, no words recognised
e. Localises pain – a limb, not necessarily one stimulated, moves toward the pain
f. Flexion to pain – pain makes elbow/knee flex, but no mvment towards painful stimulus
g. Extension to pain – pain makes elbow/knee straighten, related joints held rigid
h. Spastic flexion – instead of straightening forcibly to pain, elbow may flex
8. Doll’s eye and caloric reflex mvments → to determine LOC
a. Anatomic basis (see diagram) →

b. Aka Occulocephalic or Vestibulo-ocular reflex
i. Normal doll’s eye reflex
1. Turn head to R → Eyes reflexly move to the L (opposite direction) provided b/stem reflexes are intact
ii. Abnormal doll’s eye reflex
1. Turn head to R but eyes stay fixed and don’t move within head OR
2. Turn head to R and eyes move disconjugately (suggestive of lateral rectus palsy)
c. Caloric reflexes
i. Lift head 30’ degrees from horizontal and instill 50 mls of ice water into ear canal
ii. Normal - Water R ear, eyes move reflexly to the R (to the ear with water) – b/stem reflexes intact
iii. Abnormal
1. Water in ear, neither eye moves (suggests b/stem reflexes damaged)
2. Water in R ear, disconjugate eye mvments eg R eye point to R, no response L eye (suggests either a medial rectus palsy in the L eye or lesion with medial longitudinal fasciculus (MLF))
Determining LOC
LOC Doll’s eye reflex Caloric reflex (more powerful)
Awake +/- + / nystagmus
Stupor + + / conjugate gaze toward water
Coma - -

Determining Cause of Stupor or Coma
R L Cause of Coma
+ - Structural lesion
- + Structural lesion
+ + Metabolic coma
- - Metabolic or structural coma

9. Management of Coma
a. First line
i. Correct ABCs
ii. IV line
iii. Blood for glucose/electrolytes etc
iv. Hx from witnesses
v. Careful exmn, focal signs, clues to cause
b. 2nd line
i. ? thiamine – if poor nutrition or signs of alcoholism
ii. ? give glucose IV – 50 mls 50% dextrose IV
iii. ? naloxone – if suspicious of narcotic o/dose
iv. ? flumazenil – if suspicious of benzo o/dose
c. While doing this
i. Call ICU team
ii. Arrange brain imaging
iii. Consider LP if brain imaging unhelpful and shows no risk of brain hernation

Summary Sheet → pg 76 of neurology manual


• Epileptic seizures – many causes, but all characterised by excessive neuronal activity, commonly followed by redcued activity
• Epilepsy is a sx, not a dis
• Common – 1/200 have epilepsy and taking anti-epileptic drugs, 1/50 lifetime incidence of at least 1 seizure
• Clinical manifestations of the seizure – depend on the spatial and temporal distbn of the excessive neuronal activity
• Sub-clinical bursts of abnormal neuronal activity also occur; detected by EEG as sharp waves or spikes (aka epileptiform activity)
• Clinical seizures – abrupt onset, self-limited, last usu <1-2 mins
• Prolonged or frequent seizures w/o full recovery betw attackes → status epilepticus
• Prolonged partial or generalised seizures may produce permanent cerebral damage
• Seizures freq occur for no apparent reason but may be triggered by hormonal factors such as menstrual cycle or stimuli such as fatigue, flashing lights or hyperventilation

Causes of Epilepsy
1. Intrinsic cerebral disturbance
a. Basic predisposition to seizures, often inherited, not assoc w demonstrable dis of brain → idiopathic epilepsy (generalised seizures)
b. Structural lesion (esp cortex) – trauma, tumors, infarct, infection, cortical dysgenesis, AV malformation, scar, hippocampal sclerosis
2. Systemic metabolic disturbance – hypoxia, hypocalcaemia, hypogly, hyponatremia, uraemia (RF), fever (children), drug use (phenothiazines, antidepressants) or withdrawal (ETOH, bnezos, barbiturates)

Idiopathic epilepsy – no underlying structural brain dis
Symptomatic epilepsy – underlying brain dis present
Cryptogenic epilepsy - presumed underlying brain dis

Differential Dx
• Syncope
• Pseudoseizures (psychogenic)
• TIAs (vertebrobasilar circ (impaired consciousness)
• ICA (sensory)

Clinical Features of Epilepsy

Classification of Seizures
1. Generalised seizures
a. Generalised convulsion (tonic/clonic, grand mal)
i. Initial stiffening (tonic phase; pt falls like a tree); up to 30s, assoc w respiratory arrest + cyanosis
ii. Limb jerking (clonic phase); may be tongue biting or urinary incontinence
iii. May be a post-ictal phase with brief coma, followed by confused state and sometimes headache
iv. May be followed by sleep
b. Absence seizure (petit mal)
i. Onset in childhood (3-10y age)
ii. Brief lapses of awareness, assoc w clonic mvments (esp eyelid flickering)
iii. No aura or post-ictal drowsiness
iv. May be precipitated by hyperventilation
v. Typical EEG abnormality – generalised 3-4Hz spike and wave abnormality
vi. 80% remit <30y
vii. 30-50% also have tonic-clonic seizures
c. Atonic seizure (epileptic drop attacks)
d. Tonic seizures (Ø clonic jerks)
e. Bilateral myoclonic jerks (not always epileptic, not always benign)
2. Partial seizures (focal seizures)
A. Simple partial seizures (consciousness retained) – tumors, AV malformation, strokes, abscesses
a. Focal motor seizures (twitching/jerkign)
i. Arise in motor cortex
ii. May be followed by temporary hemiparesis (todd’s paresis) – temporary metabolic exhaustion
iii. Types –
1. Localised (foot, head, mouth)
2. Jacksonian march
3. Versive (head turning)
4. Benign rolandic (see later)
5. May see focal motor status epilepticus (epilepsia partialis continua) with ongoing motor activity and no alteration in LOC
b. Focal sensory
i. Somatosensory (localised or Jacksonian march)
ii. Visual (uniformed spots or lights)
iii. Auditory (uniformed sounds)
c. Benign Rolandic Epilepsy
B. Complex partial seizures (pt loses awareness of their surroundings)
a. Temporal lobe seizures (see below)
b. Frontal lobe epilepsy
c. Parietal lobe epilepsy
d. Occipital lobe epilepsy

Epileptic Syndromes
1. Characterised by partial seizures (see above)
a. Temporal lobe epilepsy – simple partial or complex partial seizures characterised by
i. Develop from childhood onwards
ii. Aura (noticed by pt)
1. visceral (nausea, epigastric rising sensation)
2. hallucinations (olfactory, gustatory, auditory, formed visual)
3. psychosensory (dreamy state, déjà vu, jamais vu, fear, exhilaration)
4. if seizure stops here, no alteration of awarness → simple partial seizure)
iii. Benign with motionless stare (noticed by observer) → oro-alimentary (lip smacking, chewing) + motor (fumbling, picking at clothes, walking, undressing) automatisms common
iv. Dystonic posturing sometimes – if unilateral; seizure usu in contralateral hemisphere
v. Note – if pt unable to communicate or understand, seizure may arise in left (dominant) hemisphere; but if seizure arises in non-dominant temporal lobe, may still be able to communicate
vi. Usu marked post-ictal confusion
vii. May progress to generalised seizure
viii. Common causes – hippocampal sclerosis, tumors (gliomas, benign tumors), angiomas, infections, trauma
b. Frontal lobe epilepsy – 20-30% of partial seizures
i. Often v short, freq at night, often occurring in clusters
ii. Usu no aura, consciounsness preserved, no post-ictal confusion
iii. Often bizarre – prominent vocalisation, violent dramatic mvments
iv. Discharge spreads rapidly, often generalise, status epilepticus common
c. Benign rolandic epilepsy (Benign childhood epilepsy with centrotemporal spikes)
i. Primary partial epilepsy (idiopathic)
ii. Differs from both TLE and FLE as not assoc w underlying structural brain dis
iii. Develops at ~10y age
iv. Seizures occur at night
v. Typical feats – incl unilateral paraesthesia of tongue and face, clonic mvments of tongue and face, speech arrest and preservation of consciousness
vi. May progress to 2ndry generalisation
vii. Children otherwise normal; seizures stop at puberty; child may have only one seizure ever
viii. EEG – freq centrotemporal spikes (arise in centre and temporal parts of brain)
2. Characterised by generalised seizures (see above)
a. Idiopathic (primary) generalised epilepsy (centrencephalic epilepsy)
i. Combinations of absence, tonic/clonic and myoclonic seizures
ii. Onset in c/hood, early adult life (major genetic component)
iii. Pt otherwise normal, normal devt, normal neuroimaging
iv. Tonic-clonic seizure occur with idiopathic generalised epilepsy AND with a partial seizure that becomes generalised - do not assume a tonic-clonic seizure is due to generalised idiopathic epilepsy unless there is a convincing hx of myoclonic jerks or a characteristic 3-4 hz spike and wave pattern on EEG
b. Absence epilepsy
i. Onset usu 3-10y
ii. Characterised by recurrent absence seizures where the pt stares and is momentarily unresponsive, Øaura, Øconfusion
iii. 30-50% also have tonic-clonic seizures, 80% remit <30y
iv. Atypical absences – clinically similar but slower onset/recovery
1. Seen with underlying brain dis eg Lennox gastaut syndr
2. 1-2 Hz spike on EEG
3. Frequently sig intellectual impairment
c. Juvenile myoclonic epilepsy
i. Myoclonic = single isolated jerks
ii. Common (5% of all epileptics)
iii. Onset during teens, lifelong tendency to seizures (usu anti-epileptic therapy for life)
iv. Frequent myoclonic jerks esp in first hr after waking from sleep (helps clinch the dx)
v. Infrequent tonic-clonic seizures, often preceded by clusters of myoclonic jerks (esp in first few mins after waking)
vi. 30-40% have absence seizures as well (but not usu clinically apparent)
vii. Sxs aggravated by sleep deprivation and alcohol
3. Others
a. Symptomatic/Cryptogenic epilepsy – in diffuse/multifocal brain dis, often many seizures types (atonic-tonic, myoclonic jerks, atypical absences); these seizures may look like those seen in idiopathic generalised epilepsy or absence epilepsy, but they are due to underlying structural brain dis
b. Febrile seizures (.38.5’C) – 3% of children 6mo-5y; ↑ incidence if f.hx
i. Most are simple (brief, symmetrical tonic-clonic convulsion);
ii. ~20% are complex; duration >15mins, recurrent during single febrile episode, focal or lateralising feats
iii. ~5% develop epilepsy; ↑ risk if complex seizures
iv. Prognosis benign when short duration symmetrical tonic-clonic convulsions
v. Seizures that are asymmetrical or last >15 mins, prognosis more sinister
Most impt localising feat of an epileptic attack is the v first sx – often called the aura

Diagnosis of Epilepsy

1. EEG
• Spontaneous and evoked brain activity recorded from the scalp → key tool
• Dx – EEG provides the only interictal sign (sens ~50% but rate of detection ↑ w repeated studies), specificity 98% (ie 2% false positive rate);
• Classfication – useful in distinguishing absence from complex partial seizures
• Etiology – detection of assoc EEG abnormalilties may suggest cause of seizures (eg focal EEG changes suggest underlying structural lesion and indicate need for brain imaging)
• Limited role for detecting structural brain dis (CT/MRI better)

• Obtain when suspicion of focal onset epilepsy
• Identify structural lesion – eg hippocampal sclerosis, neuronal migration d/o etc
• Not reqd in a person you suspect has primary generalised epilepsy based on the clinical feats → obtain EEG instead
• If EEG shows evidence of a generalised epileptic syndr, brain imaging not reqd
• If EEG shows focal abnormalities, neuro imaging reqd
• MRI superior to CT
• CT may be used in emergency screening situation

Management of Epilepsy

1. General Principles
a. Safety – during seizures (move objects away, recovery position, no objects in their mouth)
b. Avoiding risky activities – eg scuba diving, mountain climbing, ?swimming, fires, bar heaters, microwave preferred, back elements on stove turn pot handles inward, always pour hot water away, don’t lock bathroom doors, shower>bath, ladders, scaffolding
c. Avoidance of precipitating factors eg sleep deprivation, alcohol
d. Education and support
2. Principles of Drug Therapy
a. Do not treat after just one seizure
b. Use correct drug for correct type of epilepsy
c. Start with 1 drug incr until pt seizure free or side effects intolerable; if unsuccessful change to another drug (overlap for 6 wks)
d. If 2 individual drugs fail – consider a combination; choose 1 for baseline and try various 2nd drugs (do not continue if no obvious benefit)
e. If this fails, be prepared to reconsider the dx (eg pseudoseizures)
f. Serum levels useful for checking compliance, unusual metabolism and suspecte toxicity; but therapeutic levels should only be used a guide
3. Pregnancy
a. Risks of uncontrolled tonic-clonic seizures greater than the risk of adverse effects
b. Teratogenicity – 2-6% risk, may be >10% on polytherapy; greatest on valproate where increased risk of spina bifida + cardiac and skeletal abnormalities
c. Folic acid before conception may reduce valproate-induced neural tube defects
d. Note – enzyme-inducing anti-epileptic drugs reduce efficacy of OCP
e. ?lamotrigine may be less teratogenic than valproate and may be considered 1st line therapy in women of childbearing potential
4. Driving
a. Must stop for 1 y unless seizure was due to unusual provocative factors unlikely to recur; may be reduced to 6 m on neurologist recommendation
b. Must stop for 6 months when drug therapy changed or reduced; if a seizure occurs, pt may drive 6 months after resuming prior therapy that worked
c. Any hx of epilepsy → permanent ban from passenger service vehicles, aambulances, vehicle recovery and heavy vehicles (only 1 yr if clearly provoked)
d. A doctor is obliged to inform a pt the LTSA rules and must inform LTSA if they suspect/knows the person continues to drive against advice
5. Prognosis
a. 40% of those seen in hosp w 1st seizure have recurrence <2y (most within 6 months)
b. 70% who have 2 seizures have a third seizure
c. ↑ risk w structural lesions or if there are epileptiform discharges on EEG

Status Epilepticus
Prolonged or freq seizures w/o consciousness betw attacks
1. Medical emergency – risk to life and permanent cerebreal damage
2. General – search for causes early on, maintain ABCs
3. IV anticonvulsants necessary, but only if pt is in true status (not recovered)
4. Use only one drug at a time

Anti-epileptic Drugs

Generalised seizures (tonic-clonic)
1. Valproate, carbamazepine or lamotrigine
2. Phenytoni or clobazam (2nd line)
3. Topiramate (3rd line)

Generalised seizures (absence seizures)
1. Sodium valproate or ethosuximde (children only)
2. Clobazam or clonazepam (2nd line)
3. Lamotrigine (3rd line)
4. NOT carbamazepine

Juvenile myoclonic epilepsy
1. Valproate
2. Clobazam or lamotrigine
3. Topiramate

Partial seizures (complex or simple)
1. Carbazamepine, Sodium valproate or Lamotrigine
2. Phenytoin or clobazam (2nd line)
3. Topiramate (3rd line)

Carbamazepine (Tegretol)
• Indications – tonic-clonic seizures, partial (simple or complex) seizures
• Ineffective for absence seizures and juvenile myoclonic epilepsy
• Dosage – start slowly (eg 100 mg nocte), ↑ dose by 100 mg every few days; give bd, usual therapeutic dose 600-1600 mg/day
• Adverse effects – rash, sedation, other cogv s.effs, hyponatremi, cardiac conduction defects, neutropenia (usu benign), liver dis
• Toxic doses → ataxia, deplopia, nystagmus
• Interactions – induces metabolism of other drugs including oral or injected contraceptives and warfarin

Sodium Valproate (Epilim)
• Broad spectrum of activity
• Dosage – usual maintenance dose in adults 800-3000 mg/day taken in 2 doses; start with 200-400 mg bd; gradually ↑ dose according to clinical response; can be induced faster than carbazamepine
• Adverse effects – nausea, weight gain, hair loss, hand tremor, LF, thrombocytopenia, pancreatitis
• Teratogenicity – neural tube defects (spina bifida); ↓ risk by taking folic acid
• Interactions – inhibits metabolism of lamotrigine

Phenytoin (Dilantin)
• Indications – tonic-clonic seizures, partial seizures, ineffective against absence seizures
• Dose – usual maintenance dose 300mg/day as single dose, metabolism is saturable so marked changes in bld levels can be produced by sml changes in dose; loading dose (either 1000mg PO or 18mg/kg IV); alternatively can be started at usual maintenance dose but therapeutic levels may not be achieved for 2-3wks
• Adv effects – cosmetic (hirsuitism, coarsening of facial feats), sedation and cogv s.effs, peripheral neuropathy, cerebellar ataxia after chr use, osteomalacia
• Toxic dose – can cause ataxia and nystagmus

Lamotrigine (Lamictal)
• Broad spectrum of activity and better tolerated than older epileptic drugs
• Indications- tonic-clinic, absence and partial seizures
• Dose – start low dose (12.5 mg/day); ↑ dose gradually every wk to achieve maintenance dose 100-400 mg/day
• Interactions – metabolism inhibited by valproate, lamotrigine dose must be lowered if these drugs used together, also interacts w carbazamepine
• Adv effects – skin rash soon after tx begins, usu well tolerated


Stroke is a syndr caused by damage to the CNS by an abnormality of its blood supply, with –
1. Sudden onset (abrupt, rapidly progressive or stepwise)
2. Focal brain damage in the terrirtory of a particular artery
3. S/S persisting >24 hrs

It is difficult to distinguish stroke subtypes clinically and tx differs by type (CT scan impt).
Dx of stroke should be made with caution if –
a. poor hx – unconscious, dysphasic, no eye witness
b. coma
c. gradual onset
d. no focal signs
e. assoc w a blackout or unexplained fever

1. Ischemic Stroke (cerebral infarct) – 85%

1. Arterial Dis – thrombus at site or embolism of thrombus to distal arteries
a. Atheroma – aortic arch, distal internal carotids, prox mca, basilar art
thrombus at site may be preceded by days/weeks of TIAs
strong assoc w CAD, HT, DM
b. Lipolyalinosis – penetrating branches of cerebral arteries → pons, deep white matter
blood vessels impregnated w a hyaline-lipid material, often chr HT
c. Other arterial diseases – dissection, vasculitis (consider in young pts w no RFs for atheroma)
2. Embolism – abrupt onset, multifocal TIAs or strokes
a. Carotid art embolus (mca), Vetrebral art (pca or cerebellar art), aca not often occluded
b. Cardiac causes – AV, rheumatic valvular dis (usu m.sten), bact endocarditis, mural thrombus post MI, card surg/catheteris, cardiomyopathy
c. Non-cardiac causes – thrombosed pulmonary veins (eg bronchiectasis)
3. ↓ Cerebral perfusion pres – global cerebral hypoxia/ischemia
a. Cardiac pump failure (acute MI/ arrhythmia) or hypovolaemic shock
b. Usu borderzone (watershed) infarcts in the periphery of major vascular supplies territories

Clinical Syndromes
1. TACI (Total Ant Circ Infarct) - internal carotid or mca
a. Focal higher cerebral dysfunction 9dysphasia, apraxia (impairment skilled/purposeful mvments), agonsia (perception of sens impairment) and
b. Homonymous visual field defect and
c. Unilateral motor and/or sensory deficit involving at least 2 of face, arm, leg
2. PACI (Partial Ant Circ Infarct) – internal carotid, mca, aca
a. 2/3 TACI components or
b. Focal higher cerebral dysfunction alone or
c. Unilateral motor/sensory deficit more restricted than a lucanar infarct (eg isolated hand involvement)
3. POCI (Post Circ Infarct) – vereebral, basilar, pca
a. ipsilateral cranial n palsy (brainstem) + contralateral motor (corticospinal tract) and/or sensory deficit (thalamus, med lemniscus, spinothal tr)
b. bilateral motor and/or sensory deficit
c. d/o of conjugate eye mvments (brain stem nuclei + interconnecting pways)
d. cerebellar dysfunction w/o ipsilateral hemiparesis (cerebellum)
e. isolated homonymous visual field defect (*Isolated homonymous hemianopia usu caused by occlusion of a pca)
4. LACI (lacunar infarct) – small penetrating arteries
a. Pure motor – isolated hemiparesis affecting face, arm, leg
b. Pure hemisensory – isolated hemisensory deficit
c. Dysarthria (disturbance of speech from paralysis, incoordination or spasticity of muscles used for speaking) or clumsy hand
d. Ataxic hemiparesis
Dx excluded if visual field defect, abnormal higher cerebellar dysfunction, signs of brain stem abnormality, impaired consciousness

Acute Mgt
1. Stroke units – NNT 16 to prevent death/dependency, no additional cost, variable availability
2. Aspirin (150-300 mg) – early tx has a small LT benefit, NNT 100, inexpensive
3. IV Thrombolysis (tPA) – beneficial if started within 3 hrs of onset stroke, 30% more likely to have favourable outcome
NNT 16 (prevent death/disability), NNT 7 (for clinical benefit)
>3 hrs → hem risk at sites of dead/soggy tis
Heparin does not alter LT outcome, but may be beneficial in some carefully selected pts

2. Intracerebral Hemorrhage – 15%

Clinical distinction betw intracerebral hem and ischaemic stroke difficult – CT reqd for this.
Indications of an intracerebral hem → hx of HT, no prodromal TIAs, severe headache, gradual onset (mins-hrs), ↓ consciousness, stiff neck

Pathophysiology (major causes – 1 and 2)
1. Hypertension – either degenerative changes in penetrating arteries due to chr HT or abrupt rise in BP
2. Cerebral amyloid angiopathy – leading cause of intracerebral hem >70 yrs age (amyloid laid down in vessel wall causing wall weakness/obstruction)
freq lobar (near surface) and often extends into subarachnoid space, tends to recur, assoc w alzheimer’s dis
3. Vascular abnormalities – Arteriovenous malformations + cavernous angiomas (common cause in young pts)
4. Tumors – 5% of intracerebral hemorrhages, primary or 2ndry, most common glioblastoma and mets
5. Bleeding d/os and anticoagulant tx - 10x ↑ risk on warfarin (esp INR >4)
6. Exogenous factors – sympathomimetic drugs (amphetamine, cocaine), trauma

1. Reverse anticoagulant therapy - Vit K + FFP (warfarin), protamine (heparin)
2. BP control – keep below 170/110
3. Surgical evacuation has limited role, indications –
cerebellar hematomas >3cm in diam who are deteriorating due to brainstem compression or hydrocephalus
pts w underlying structural lesion, aneurysm, arteriovenous malformation, cavernous angioma
4. ↓ ICP – furosemide, hyperventilation, mannitol
5. Potential role for recombinant F7 in future – early trails suggest improved outcome if tx <4 hrs
Corticosteriods – to tx inflam and ↓ ICP → ineffective

3. Subarachnoid Hemorrhage - <5%

Epidem F>M, annual incidence 1/10K, incidence has not declined over last 30 yrs, case fatality rate for aneurismal subarac hem has not changed

Pathophy Most due to rupture of a sacular (berry) aneurysm – arteriovenous malformation is an occasional cause – 10-20% of cases, no source of bleeding found
Aneurysms occur at sites of arterial wall weakness esp term int carotid, mca, ant communicating arts (5% of popn affected but only 10% of these rupture)
Slowly ↑ in size, but gen asx until rupture

Pres Thunderclap headache (abrupt onset typically during exertion)
Vomiting +/- loss of conciousness
Meningism (sxs mimicking meningitis but no acute inflam present) impt sign – but may take hrs to develop
Focal signs not prominent

Ixs Urgent non-contrast brain CT – pos in 90% (within 24 hrs) – after 1 wk, CT often neg
Lumbar puncture in all CT neg pts 6-12 hrs – CSF shows rbcs, xanthocrhomia at 12 hrs
Cerebral angiography – to localise aneurysm or AV malformation w view to clipping (aneurysm) or excision (AVM)
MRI not sensitive in detecting acute subarach hem

Mgt 15% pts die pre-hosp, 10% die day 1, 1/3 die within next 3 months
Definitive tx = isolation of offending aneurysm from cerebral circ as high risk of re-bleeding if left untx
Surgical clipping of aneurysm
Some aneurysms may be occluded by inserting detachable coils and balloons into aneurysm through a catheter
Deterioation 1-2 wks follow subarac hem may be due to narrowing and/or spasm of cerebral arteries often leading to infarction – prevent by using CCBs
BP control debateable – high BP causes rebleeding v hypoperfusion infarct from low BP

Assessment and Mgt of Stroke

Diagnostic Approach
1. Is it a stroke?
2. Where is the lesion?
3. Which type of lesion is it?
4. What is the underlying cause?
5. What are the functional consequences?

Clinical Assessment
Hx – esp onset and progression of sxs
Neuro exam – where is lesion?
Gen exam – BP both arms, heart, pulse carotid bruits, fundi

Ixs Bloods FBC – anemia, polycythemia, thrombocytopenia, thrombocytosis
ESR - ↑ in endocarditis, vasculities
E/lytes, creatinine, glucose
Brain imaging Non-contrast CT (differentiate ischemic and hemorrhagic strokes and separate out differentials)
MRI scans more info (can perform MRI angiography at same time) – identify cerebral infarct first few hrs when CT appearance subtle
Selected pts w ischemic stroke Vasculitic or thrombophilia screen (young pts w ischaemic stroke)
Blood cultures (if suspected bact endocarditis)
CXR if clin indic
Echo – if abnormal cardiac exam, ECG or CXR)
Imaging of carotid and cerebral arteries
Selected pts w hem stroke Coagulation studies
Angiography/MRI angiography

Primary Prevention
1. Modify RFs – anti-HT, smoking cessation, DM control, exercise, low cholesterol
2. Warfarin – prosthetic heart valves, AF, rheumatic valvular dis, hypercoaguable states
3. Surgery – controversial (asx endarterectomy, aneurysm AV malformations)
Endartrectomy – excision of atheromatous deposits + diseased endothelium/media to leave the artery w a smooth lining (adventitia)
2ndry Prevention
1. Lifestyle RFs – smoking cessation, restricted alcohol consumption, moderate exercise, weight loss
2. Anti-platelet therapy (aspirin) – used in all people w ischemic stroke/TIA unless indication for anti-coag (eg AF) or contra – dose 75-150mg
Aspirin + Dipyridamole → greater benefit (dubious evidence) - only funded if allergic to aspirin or had a stroke/TIA while on aspirin
Clopidogrel appears ineffective
3. Warfarin – stroke/TIA pts w non-valvular AF, rheumatic valvular dis, mech heart valves or recent MI
4. Anti-hypertensives – ↓ BP ↓ risk of recurrent stroke (+ oth maj vasc events) for all stroke/TIA pts – irrespective of the person’s baseline BP
5. Lipid lowering therapy – statin should be used for most people w stroke/TIA – also irrespective of person’s baseline cholesterol
6. Tx of DM – diet, oral hypoglycemics, insulin
7. Carotid endarterectomy in pts w ipsilateal internal carotid stensoses

1. Neurological
a. Cerebral edema – 24-48 hrs after large hemispheric ischaemic/hem stroke (assoc w poor prog)
avoid aggravating factors - hypo-osmolar fluids, hypoxia, CO2 retention, fever, ↑ CVP, agitation
osmotic diuretics (mannitol) may reduce ICP temporarily, steroids are not beneficial
b. Hydrocephalus and brainstem compression – swelling assoc w cerebellar infarction or intracerebral hem can compress the brain stem or cause
acute hydrocephalus - 1-4 days post cerebellar stroke → ventr drainage and surgical decompression may be reqd
c. Seizures – tx w anticonvulsants (may not necessarily lead to chr epilepsy)
2. Systemic
a. DVT/PE – 50% of pts w hemiplegia following stroke
Heparin sc reduces risk of DVT/PE after acute ischaemic stroke (hem and GI bleeding risk), DVT stockings, early mobilisaiton
b. BP HT – inpaired cerebral autoreg in acute phase of stroke, avoid ↓ BP first few days post stroke as may ↑ size of an ischemic stroke
Hypotension – commonly due to dehydration, anti-HT meds
c. Metabolic Hypoxia – commonly due to aspiration pneumonitis, a/way obstr, hypovent – give O2 and protect airway w ET if indic
Hyponatremia – commonly due to SIADH causing acute confusional state, seizures
d. Fever and Inf (esp lung and urinary tract) – common cause of mortality

Prognosis 20% die first month after stroke
55% dead/dependent at 1 yr
Recurrent risk of stroke – 10% in first 6 months (5% per year after this)

Transient Ischaemic Attack (TIA)

TIAs caused by temporary cessation of blood flow to part of brain or retina – often due to microembolism, (rarely - vasospasm or transient hypotension)
Sxs resemble stroke but resolve within 24 hrs (usu 2-15 mins)
TIAs may be the precursor of ischaemic strokes
TIAs do not precede a intracerebral hem nor cause a LOC
ITIAs are not suggested by – solated focal sxs such as dizziness, double vision, dysphagia
Non-focal sxs such as faintness, dizziness, confusion

Etiology Large art dis (usu atheroma) 50%, cardiac emboli 10%, Misc causes 15%, Idiopathic 25%)

Feats Sxs depend on site –
Carotid art (usu mca brs) – weakness, numbness, aphasia
Ophthalmic art – transient monocular blindness
Vetrebral/Basilar art – dizziness, diplopia, dysarthria, facial numbness or weakness, ataxia, blurred vision

Prognosis 25% of pts have an adverse in the 3 months following a TIA (10% have a stroke in the following 2 days)
ABCD (2) Score (Risk of Stroke following a TIA)
Age >60 1
BP at 1st assessment – sys >140/dias>90 1
Clinically unilat weakness 2
Or Speech dysfunc but no mus weakness 1
Duration 10-59 mins 1
>60 mins 2
DM 1
Admit pt to hospital if a score of 4+ or if young – to ensure ixs done and 2ndry prev initiated

Carotid Bruits

Often assoc w stenosis at the origin of the ICA (bruit maximal at angle of jaw)
May arise from ECA and are not specific or sensitive for stenosis
Severe stenoses may not cause a bruit
Risk of stroke – 1-2% / year


Other causes of turns or blackouts that may be mistaken for epileptic turns; note not all seizures are due to epilepsy

Collapse with loss of consciousness

A. Syncope
1. Loss of function due to abrupt global reduction of blood flow to brain
2. Sxs
a. Dizzy, lightheaded
b. Vision may blackout with transient retention of awareness
c. Sounds may be quiet, distant, muffled
d. Looks pale
e. Eyes roll back
f. Person slumps to the floor
g. Pulse may be weak or thready
h. May have a few muscle twitches or v brief convulsions (convulsive syncope); minimal postictal confusion; often misdx as epilepsy
3. Causes
a. Vasodepressor (vasovagal) syncope or simple faint (often triggered by strong emotional circumstances)
b. Cardiac d/os eg. arrhythmias or pump failure
c. Peripheral pooling of blood eg after arising suddenly from lying or sitting positions or prolonged standing; can be precipitated by meds
d. Hypovolemia eg. blood loss
e. Sudden – intrathoracic pressure ↓ VR to heart eg prolonged coughing (cough syncope), valsalva manoeuvre, micturition (usu when men arise at night to urinate)

Syncope vs Grand Mal Seizure
Fit (seizure) Faint (syncope)
Mechanism Generalised seizure with paroxysmal electr d/c Loss of function due to abrupt ↓ cerebral perfusion
Precipitating Circumstances None; not related to posture Common; prolonged upright, emotion, severe pain, hot evt, medical evt, illness, preg
Speed of onset Abrupt Usu gradual (secs-mins)
Prodrome Usu none Faintness, nausea, salivation, pallor, sweating, cold, fading vision, yawning, sighin, tinnitus, muffled hearing, may avert attack by lying down
Attack +/- initial partial seizure
Crashes stiffly
Tonic-clonic convulsions
+/- urinary incontinence
+/- cyanosis
Injury common Slumps limply
Eyes often rolled up
+/- brief jerking face
Urinary incontinence uncommon
Pallor +/- flushing during recovery
Injury uncommon
Post-ictal Slow recovery
Confusion, drowsiness
Tongue bitten Rapid recovery – secs-mins (occasionally longer esp if kept upright) +/- postural faintness

B. Non-Epileptic attacks
• Often very difficult to identify and need a high degree of suspicion
• Highly variable attacks
• Often tearful following seizure
• Often late onset
• Resistant to tx
• Odd beh (eg overly familiar or aggressive)
• Often hx of abuse
• Made more complicated as often a hx of epilepsy

C. Drop Attacks
• Usu occur in elderly women
• Attacks occur while pt is standing or walking
• W/o warning, knees buckle and pt falls forward
• +/- transient LOC
• May suffer injuries to knees and face
• Recovery immed
• Cause unknown; may be 2ndry to TLE or cardiac arrhythmia; often attributed to brain stem ischemia but little evidence to support this hypothesis

B. Funny turns without loss of consciousness

A. Migraine Aura
• Clinical feats that suggest an episode of focal neurological sxs is a migraine aura
• Young
• Past Hx of migraine
• F.hx migraine
• Positive sxs
• Visual – flashes of light, zigzags, scintillations, fortification spectra
• Sensory – tingling, pins and needles
• Sxs develop gradually over 5-20 mins; may spread from one part to another
• Sxs may not follow the vascular territory of a single artery
• May be followed by headache, but not always

B. Panic Attacks / Hyperventilation Syndrome
Sxs of hyperventilation vary markedly betw individuals
• Sxs may incl
• Feelings of dread, unreality and panic
• Palpitations
• Constriction of throat and chest
• ↑ resp rate
• sweating
• Tremulousness
• Tingling in lips, hands and feet
• Carpopedal spasm
• Sensory sxs are usu bilateral, but can be unilateral (esp affecting the L side of the body)
• Sxs may recur many times a day or infreq
• Sxs often occur in circumstances in which there is no obvious source of fear
• Attacks may awaken pts from sleep
• Many pts have similar but milder sxs in betw acute attacks; fatigue, breathlessness, freq sighing, nervousness, dizziness, headache


D. Hypoglycemia



Gen Med Core Topics
• Sxs characterising stroke from other disorders and where lesion likely to be found
• Acute mgt of stroke – first 48 hrs re assessment, ixs and tx
• Mgt of BP and chol LT w view to stroke recurrence avoidance
• Merits of warfarin tx in stroke – primary + 2ndry prevention

1. Definition
a. Syndrome caused by damage to the CNS by an abnormality of its blood supply AND -
i. Sudden onset
ii. Focal brain damage in the territory of a particular artery
iii. S/S >24 hrs
2. Ischemic Stroke – 85%
a. Pathophysiology → cerebral infarction
i. Thrombosis at site of an atheromatous plaque (major cerebral vessel or small vessel deep in brain)
ii. Emboli arising from –
1. atheromatous plaques in carotid/vetrebrobasilar arteries
2. cardiac mural thrombi – eg post MI, AF, rheumatic valvular dis
iii. Global hypoxia/ischemia (↓ cerebral perfusion) → cardiac pump failure (acute MI, arrhythmia, hypovolaemic shock)
b. Major RFs for thromboembolic stroke – same as those for atheroma
i. HTN, DM, Smoking, hyperlipidemia, obesity, OCP, 2ndry polycythemia
c. Clinical Syndromes
i. TACI (total arterial circ infarct) → Internal carotid or MCA
1. Focal higher cerebral dsyfuntion – dysphasia (dominant hemisphere) or apraxia or agnosia (non-domin)
a. Apraxia – impairment in skilled mvments
b. Agnosia – inability to recognise
2. + Homonymous hemianopia (optic radiation) – note that isolated homon.hemianopia usu caused by POCI
3. + Unilateral motor/sens defect – 2 of face/arms/leg (motor or somatosensory cortex)
ii. PACI (partial arterial circ infarct) → Internal carotid, MCA or ACA
1. 2/3 of a TACI
2. OR focal higher cerebral dysfunction alone
3. OR unilateral motor/sens defect eg hand alone
iii. POCI (posterior circ infarct) → vertebral, basilar, PCA
1. Ipsilateral CN palsy + contralateral motor/sens deficit
2. Bilateral motor/sens deficit
3. Disconjugate eye mvments
4. Cerebellar dysfunction
5. Isolated homonymous hemianopia
iv. LACI (lucanar infarct) → small penetrating arteries
1. Pure motor deficit
2. Isolated hemisensory deficit
3. Dysarthria
4. Ataxic hemiparesis
d. Acute Management
i. Stroke Unit
ii. Aspirin
iii. IV thrombolysis – tPA <3 hrs (later and risk of hemorrhage at sites of dead tis)
iv. Intra-arterial thrombolysis – may be effective if started <6 hrs in selected pts w large vessel occlusion – ICA, MCA, basilar
v. Heparin – usu not beneficial
vi. Supportive care – prevent, identify and tx complications rapidly
3. Clinical Features (kumar)
a. Cerebral hemisphere infarcts
i. Internal capsule infarct – motor and sensory fibers converting on brainstem from cerebral cortex
1. Blood vessel – branch of MCA
2. Features
a. Contralateral hemiplegia
b. Hemisensory loss
c. UMN facial weakness
d. Hemianopia
3. Signs
a. Initially – hypotonic hemiplegia w ↓ reflexes
b. Within days – develops into a spastic hemiplegia w ↑ reflexes + extensor plantar response (UMN lesion)
ii. Brainstem infarction
1. Posterior inferior cerebellar art occlusion
a. Sudden vertigo and vomiting
b. Ipsilateral horners syndrome
c. Facial numbness
d. Cerebellar signs
e. Palatal paralysis
f. Diminished gag reflex
2. Coma – involvement of reticular formation
3. Pseudobulbar palsy – lower b/stem infarction
4. Intracerebral (cerebral) hemorrhage – 15%
a. Pathophysiology
i. HTN → degeneration of penetrating arteries or abrupt ↑ in BP
ii. Abrupt ↑ in BP → hemorrhage
iii. Cerebral amyloid angiopathy – leading cause if >70 yrs (amyloid laid down in wall → weakness, obstruction)
iv. Vascular abnormalities – arteriovenous malformations and cavernous angiomas – young pts
v. Coagulation therapy – warfarin 8-11x ↑ risk compared to those not receiving anti-coagulants (risk esp if INR >4)
vi. a
b. Presentation
i. Hx of HTN
ii. No prodromal TIAs
iii. Severe headache
iv. Gradual onset (mins-hrs)
v. ↓ conciousness
vi. Stiff neck
c. Ixs
i. CT reqd to differentiate hemorrhagic from ischemic strokes
d. Management
i. Reverse anticoagulant therapy
1. Protamine (heparin)
2. Vit K, FFP (warfarin)
ii. BP control – keep below 170/110
iii. Surgical evacuation only role if -
1. cerebral hematomas >3cm + deterioration due to b/stem compression
2. pts w underlying structural lesion aneurysm, AV malformation or cavernous angioma
iv. ↓ ICP – furosemide, hyperventilation, mannitol
5. Subarachnoid hemorrhage - <5%
a. Epidem – F>M, 1/10K per year, incidence is not declining
b. Etiology – rupture of secular berry aneurisms
c. Presentation
i. Thunderclap headache
ii. Vomiting
iii. Meningism
iv. +/- ↓ LOC
d. Ixs
i. Urgent non-contrast CT (positive in 90% in 1st 24 hrs, declining so often negative after 5-7 days)
ii. Lumbar puncture if normal CT → ↑ numbers rbcs and xanthochromia (after 12 hrs)
iii. MRI Ø sens
iv. Cerebral angiography → localise vascular problem (aneurysm or AV malformation)
e. Tx
i. Surgical clpping of aneurysm (high risk of re-bleeding if left untx)
6. Clinical Assessment
a. Bloods
b. ECG
c. Non-contrast CT
d. MRI or MR angiography
e. Optional ischemic
i. Vasculitic or thrombophilia screen (in young pts)
ii. Blood cultures
iii. CXR
iv. Echo
v. Carotid and cerebral artery imaging
f. Optional hemorrhage
i. Coagulation studies
ii. Angiography/ MR angiography
7. Emergency Management (Kumar)
a. Ixs
i. Brain CT (or MRI)
1. Site of lesion
2. Distinguish betw ischemic and hemorrhagic strokes
3. Identify mimicking conditions – eg cerebral tumor or abscess
ii. INR
iii. ECG – MI or AF
b. Tx
i. Aspirin 300 mg daily – given as soon as hemorrhage excluded
ii. Thrombolysis – IV tPA improves functional outcome if <3 hrs of ischemic stroke
c. Supportive care
i. Stroke unit
ii. Swallowing and Feeding
iii. Physiotherapy
8. Prevention
a. Primary prevention
i. RF modification
1. Anti-HTN - ↓ risk for both ischemic and hemorrhagic strokes
2. Ø smoking
3. DM control
4. Exercise
5. ↓ cholesterol - statins
ii. Warfarin
1. Mechanical heart valves
2. AF
3. Rheumatic HD
4. Hypercoagulant states
iii. Surgerical endarterectomy (excise atheromatous deposits + diseased endothelium → leave smooth lined adventitia)
1. If >70% stenosis + no recent neuro sxs (ie axs carotid stenosis)
iv. a
b. 2ndry prevention
i. Lifestyle RFs – smoking, alcohol, exercise, weight loss
ii. Aspirin 75 mg daily (clopidogrel if aspirin intolerant) – unless warfarin indicated
1. Aspirin + Dipryidamole combination of benefit but dipyridamole only funded if pt allergic to aspirin or has stroke while taking aspirin
iii. Warfarin – For those with Stroke/TIA + AF, Rheumatic HD, mechanical valves, MI (NNT = 12 over 1 year)
1. Start >14 days after onset ischemic stroke as bleeding may occur into infracted area
iv. Anti-HTN – all pts irrespective of baseline BP (start >14 days post stroke)
v. Statin – for most pts
vi. DM optimal control
vii. Carotid revascularisation – considered for pts with ipsilateral (same side as stroke/TIA) internal carotid artery stenosis
1. Carotid endarterctomy - ↓ risk of recurrent stroke (by 75%) if stroke + narrowed lumen by >70%
9. Stroke Complications
a. Neuro
i. Cerebral edema – 24-48 hrs post stroke
ii. Hydrocephalus + b/stem compression – 1-4 days post storke
iii. Seizures
b. Systemic
i. DVT/PE → DVT stockings, early mobilisation + heparin
ii. HTN –I impaired cerebral autoregulation during acute phase of stroke
iii. Fever + infection – esp lung
10. TIA
a. Definition
i. Temporary cessation in cerebral supply
ii. Micro-embolism – form atheramatous plaques or cardiac mural thrombi
iii. Sxs resemble stroke but resolve <24 hrs
iv. May be a precursor of ischemic strokes
b. Presentation
i. Carotid artery → weakness, numbness, aphasia
ii. Ophthalmic artery → transient mono-ocular blindness (amarosis fugax)
iii. Vetebral/basilar artery → dizziness, diplopia/blurred vision, dysarthria, facial weakness/numbness, ataxia
c. Risk of stroke following TIA → ABCD Score (admit if 4+ or young)
i. Age >60 1
ii. BP >140 / >90 1
iii. Clinically Unilat weakness 2
Speech dysfunc 1
iv. Duration 10-59 mins 1
>60 mins 2
v. DM 1


1. Definitions
a. Epilepsy – any of various disorders characterised by excessive neuronal activity and where clinical manifestations depend on the spatial and temporal distribution of the increased activity
b. Idiopathic epilepsy – no underlying structural brain disease
c. Symptomatic epilepsy – underlying brain dis present
d. Crytpogenic epilepsy – presumed underlying brain dis
e. Epileptiform activity – subclinical bursts of abnormal neuronal activity detected on EEG as sharp waves or spikes
f. Myoclonic – single isolated jerks
g. Status epilepticus – prolonged or frequent seizures w/o full recovery betw attacks
2. Etiology
a. Intrinsic cerebral disturbance
i. Idiopathic epilepsy - predisposition to seizures not assoc w demonstrable brain dis, usu inherited
ii. Structural lesion – eg trauma, tumours, infarct, infection, hippocampal sclerosis
b. Systemic metabolic disturbance
i. Eg – hypoxia, hypocalcemia, hypoglycaemia, hyponatremia, uraemia, fever (children), drug use, ETOH withdrawal
3. Differentials
a. Syncope
b. Pseudoseizures (psychogenic)
c. TIAs (impaired conciousness)
4. Classification of seizures
a. Generalised
i. Generalised convulsion (tonic-clonic, grand mal) – initial tonic phase, then clonic phase, post-ictal drowsiness/coma then confused state +/- headache
ii. Absence (petit mal) – brief lapses in awareness, assoc w clonic mvments (eg eyelid flickering), Ø aura or post-ictal drowsiness, onset childhood (3-10 yrs), 80% remit <30 yrs age, 30-50% have tonic-clonic seizures
iii. Atonic (drop attack)
iv. Tonic seizures (Ø clonic jerks)
b. Partial (focal)
i. Simple (consciousness retained)
1. Focal motor seizures (twitching-jerking)
a. Arise in motor cortex, may be followed by temporary hemiparesis (Todd’s paresis)
b. Types – Localised (foot, head, mouth), Jacksonian march
2. Focal sensory seizures – somatosensory, visual (eg spots), auditory (eg uniformed sounds)
3. Benign rolandic epilepsy
ii. Complex (consciousness lost)
1. Temporal lobe seizures
2. Frontal lobe seizures
5. Epileptic Syndromes
a. Characterised by partial seizures
i. Temporal lobe epilepsy
1. Aura
a. Visceral – nausea, epigastric rising sensation
b. Hallucinations – olfactory, auditory
c. Psychosensory – dreamy state, dejavu, jamais vu (Ø recog something familiar)
2. Note - If seizure stops here with no alteration of awareness → simple partial seizure
3. Begins with motionless stare then –
a. Oro-alimentary autisms (lip smacking, chewing)
b. Motor autisms (fumbling, picking at clothes)
4. Usu marked post ictal confusion
5. May progress to generalised seizure
6. Common causes – hippocampal sclerosis, tumors, infections, trauma
ii. Frontal lobe epilepsy
1. Short, frequently at night
2. Features – often bizarre eg prominent vocalisation, violent dramatic mvments
3. Often genralise
4. Consciousness retained, no post ictal confusion
iii. Benign rolandic epilepsy
1. Primary partial childhood epilepsy, differs from TLE and FLE as no underlying structural brain dis
2. Develos ~10 yrs age
3. Clinical features
a. Typically nocturnal seizures
b. Unilateral paraesthesia of tongue/face, clonic mvments of tongue/face, speech arrest, preservation of consciousness
c. May progress to 2ndry generalisation
4. EEG – freq centrotemporal spikes
b. Characterised by generalised seizures
i. Idiopathic generalised epilepsy
1. Combinations of absence, tonic/clonic and myoclonic seizures
a. Tonic-clonic seizures may be due to 2ndry generalisation of a partial seizure – do not assume a tonic clonic seizure is due to generalised idiopathic epilepsy unless convincing hx of myoclonic jerks or characteristic 3-4 hz spke and wave pattern on EEG
2. Onset in childhhod and early adult life – genetic component
3. Pt otherwise normal – normal devt and neuroimaging
ii. Absence epilepsy
1. Onset usu 3-10 yrs age
2. Recurrent absence seizures (staring and momentarily unresponsive)
3. Ø aura, Ø confusion
4. 30-50% also have tonic clonic seizures
iii. Juvenile myoclonic epilepsy
1. Common – 5% of all epileptics
2. Onset during teens, lifelong tendency to seizures
3. Features
a. Freq myoclonic jerks – esp first hr after waking from sleep
b. Infrequent tonic-clonic seizures (often preceded by a cluster of myclonic jerks)
4. Sxs aggravated by sleep deprivation and alcohol
6. Diagnosis
a. EEG
i. Sensitivity 50% but rate of detection ↑ with repeated studies
ii. Specificity 98% - only 2% false positive rate
iii. If EEG shows focal abnormalities → MRI reqd
b. MRI
i. When suspicion of focal onset epilepsy – not reqd when you suspect primary generalised epilepsy from clinical feats
ii. Identification of structural lesion – eg hippocampal sclerosis
c. CT – emergency detection, inferior to MRI
7. Management
a. General principles
i. Safety during seizures – move objects away, no objects in mouth, recovery position
ii. Avoid risky activities – eg scuba diving
iii. Avoid precipitating factors – eg sleep deprivation, alcohol
iv. Education and support
b. Drug therapy
i. Ø after just one seizure
ii. Start 1 drug - ↑ dose until pt seizure free or side effects intolerable
iii. If unsuccessful – switch to another drug (overlap for 6 weeks)
iv. If 2 drugs fail – combination (1 baseline + try various 2nd drugs)
v. Correct drug for type of epilepsy
1. Valproate – 1st line for all types
2. Carbazamepine and Lamotrigine – 1st line for generalised tonic-clonic and partial seizures
a. Ø for generalised absence seizures
3. Phenytoin – 2nd line for generalised tonic-clonic and partial seizures
c. Pregnancy
i. Risks of uncontrolled tonic-clonic seizures outweigh teratogenecity risks
ii. Teratogenecity – 2-6% (10% if polytherapy) – highest on valproate where ↑ risk spina bifida, cardiac and skeletal abnormalities
iii. Lamotrigine appears less teratogenic and considered 1st line in pregnancy
iv. Add folic acid before conception to reduce risk of neural tube defects
d. Driving
i. Ø 1 yr (6 months if unusual provocative factorunlikely to recur and neurologist recommendation)
ii. Ø 6 months when drug therapy changed or reduced
iii. Hx of epilepsy – permenant ban from passenger service/heavy vehicles etc
iv. Dr obliged to inform pt of rules and LTSA if advice not taken
8. Prognosis
a. 40% recurrence within 2 yrs after first seizure (usu <6 months)
b. Those who have had 2 seizures have a 70% risk of a 3rd seizure

Turns and Blackouts

1. Collapse + loss of consciousness
a. Differential Dx → seizure, syncope, drop attack, psychogenic
b. Syncope
i. Def – loss of function due to abrupt global reduction blood flow to brain
ii. Etiology
1. Vasovagal syncope (simple faint)
2. Cardiac d/os – eg arrhythmia, pump failure
3. Peripheral pooling of blood – eg standing suddenly from lying, prolonged standing
4. Hypovolaemia
5. Sudden intrathoracic pres ↓ VR to heart (eg prolonged coughing, valsalva)
iii. Sxs
1. Dizzy, light headed
2. Vision may blackout
3. Sounds quiet, distant, muffled
4. Pale
5. Eyes roll back
6. Slumps to floor
7. Pulse weak or thready
8. Often mistaken for epilepsy – as may have a few muscle twitches or brief convulsion, minimal post-ictal confusion
Syncope vs Grand Mal Seizure
Fit (seizure) Faint (syncope)
Mechanism Generalised seizure with paroxysmal electr d/c Loss of function due to abrupt ↓ cerebral perfusion
Precipitating Circumstances None; not related to posture Common; prolonged upright, emotion, severe pain, hot evt, medical evt, illness, preg
Speed of onset Abrupt Usu gradual (secs-mins)
Prodrome Usu none Faintness, nausea, salivation, pallor, sweating, cold, fading vision, yawning, sighin, tinnitus, muffled hearing, may avert attack by lying down
Attack +/- initial partial seizure
Crashes stiffly
Tonic-clonic convulsions
+/- urinary incontinence
+/- cyanosis
Injury common Slumps limply
Eyes often rolled up
+/- brief jerking face
Urinary incontinence uncommon
Pallor +/- flushing during recovery
Injury uncommon
Post-ictal Slow recovery
Confusion, drowsiness
Tongue bitten Rapid recovery – secs-mins (occasionally longer esp if kept upright) +/- postural faintness

c. Drop attack
i. Elderly women typically
ii. While pt standing or walking → knees buckle and pt falls forward w/o warning (+/- transient ↓ LOC)
iii. Immediate recovery
iv. Cause unknown
d. Non-epileptic attack (psychogenic)
i. Highly variable attacks, often emotional, late onset, resistant to tx, odd beh, hx of abuse, may be complicated by epilepsy hx
2. Funny turns w/o loss of consciousness
a. Migraine aura
i. Visual aura – flashes of light, zig zags etc
ii. Sensory aura – tingling, pins and neddles
iii. Sxs develop over 5-20 mins
iv. +/- followed by headache
b. Panic attack
c. TIA
d. Hypoglycaemia

Acute Confusion

Acute Confusional State
1. Defintion
a. Global impairment of higher function due to bilateral dysfunction of both hemispheres
b. Developing over hours
2. Etiology
a. Systemic or metabolic d/o (most common – esp elderly and hospitalised pts)
i. Drugs
ii. Acute systemic illness – eg pneumonia, UTI
iii. Oran failure – uraemia, LF, HF, respiratory failure
iv. Hypoxia, Hypercapnia
v. Acid-base abnormalities
vi. Electrlyte abnormalities
vii. Hypoglycaemia
b. Acute bilateral cerebral hemisphere dis
i. Infection s- eg meningitis, enchalitis
ii. Subarachnoid hemorrhage
iii. Head injury
iv. Seizure
c. Focal mass lesions, ↑ ICP and shift of intracranial contents
i. Infarction with edema
ii. Intracerebral hemorrhage
iii. Subdural hematoma
iv. Tumour
v. Abscess
3. Clinical features
a. Reduced speed and clarity of thinking
b. Drowsiness
c. Inattention
d. Disorientation
e. Illussions
f. Impaired memory
4. Exmn
a. Assessment of cogv function – speech, orientation, memory
b. Neurological exam – papillodema (↑ ICP), VFs, pupil/eye mvments, focal weakness
c. General medical exam – temp, systemic dis, neck stiffness/meningism (infection or subarachnoid hemorhage)

1. Definition
a. In neurology - a form of confusional state with additional features of –
i. Agitation – eg pulling tubes
ii. Tremulousness
iii. Autonomic overactivity
iv. Visual hallucinations
v. convulsions
b. Delirium tremens – classical form of delirium
2. Etiology
a. Any of the conditions causing acute confusional state
b. Drugs – amphetamines, steroids (prednisone high dose)
c. Withdrawal – ETOH, benzos
d. Acute infections

Acute confusional state and Delirium
1. Differentials
e. Psychiatric – eg psychosis
f. Dementia – longer onset, but may be pre-existing and unrecognised
2. Ixs → search for the cause
g. FBC, Na, calcium, Creatinine, LFTs, glucose
h. ABGs
i. Blood cultures, urine examination, urine drug screen
j. CXR
3. Mgt
k. Tx underlying cause – stop any drugs that may be causing confusional state
l. Environment – prevent injury, optimal stimulation
m. Avoid sedation if possible – clonazepam or haloperidol may be reqd if delirious/agitated (ie thrashing about etc)

Stupor and Coma

1. Definitions
a. Drowsiness → Stupor → Coma
b. Stupor – sleep like unresponsivenss from which pt may temporarily be aroused through vigorous and repeated stimulation
c. Coma – pt cannot be roused, not responsive to external stimulation
2. Etiology
a. Structural
i. Infratentorial – 15% causes of coma → lesion affecting RAS in upper b/stem
1. Causes
a. Vascular (occlusion of basilar artery or hemorrhage into pons/midbrain) – most common
b. Cerebellar tumour
2. Hx
a. Sudden or subacute onset
b. Diplopia
c. Ataxia
d. Vertigo
e. N/V
f. Headache
ii. Supratentorial – 20% causes of coma
1. Mass lesion in cerebral hemisphere affects RAS indirectly as a result of herniation of brain substance
a. Swollen brain herniates across midline and down through the tentorial notch
b. Upper b/stem is stretched and compressed
2. Causes
a. Intracerebral hemorrhage
b. Large ischemic stroke with edema
c. Subdural or extradural hematoma
d. Brain tumour
e. Brain abscess
3. Presentation
a. s/s of focal brain dis – eg headache, hemiparesis, aphasia etc
b. bilateral umn signs – eg ↑↑ plantars
c. signs of ↑ ICP – papilledema, cushings sign (↑ BP + relative bradycardia)
b. Diffuse, multifocal or metabolic – 65%
i. Etiology
1. O2 deprivation or substrates – eg hypoxia, hypoglycaemia
2. Organ dis (other than brain)
3. Endogenous poisons incl drugs – eg sedatives
4. Electrolyte or acid base disturbance – eg hyponatremia, hypernatremia, m.acidosis
5. Infection or inflammation – eg meningitis, encephalitis
6. Others – post-seizure, head injury, subarachnoid hemorrhage
ii. Presentation
1. Gradual or progressive onset (except subarachnoid hemorrhage or infection)
2. Symmetrical neuro findings
3. Pupillary reactions to light usu retained (even if other b/stem ocular reflexes (dolls eye, caloric) are lost)
3. Differential Dx
a. Locked in syndrome
i. Paralysis of arms, legs, facial, bulbar muscles (cant speak, move tongue or swallow)
ii. Vision, hearing and somatosensory hearing intact
iii. Vertical eye mvments intact
b. Psychogenic unresponsiveness
4. Assessment of a comatose pt
a. ABCs
b. Determine LOC
c. GCS
d. Determine cause of coma
i. Witness hx
ii. Exmn
1. Respiratory pattern
a. Hypopnea – metabolic coma (drug od)
b. Hyperpnea – central neurogenic hypervent, m.acidosis, hypoxia
2. Pupillary light reactions
a. Normal pupils – metabolic coma
b. Unilateral pupil dilation – transtentorial herniation
c. Mid position and fixed pupils – midbrain lesion
3. Reflex eye mvments → to determine if b/stem reflexes are intact
a. Doll’s eye reflex (vestibule-ocular reflex)
i. Normal – turn head to R, reflex eye mvment to the L
ii. Abnormal – eyes stay fixed and move with head or eyes move disconjugately suggesting a eye muscle palsy
b. Caloric reflexes
i. L head 30’ from horizontal and instill 50 mls ice cold water into ear canal
1. Normal – water R ear, eyes move to the R (the ear with the water)
2. Abnormal – neither eye moves (b/stem reflexes damaged) or unilateral respose indicating a rectus palsy or lesion of MLF (med long faciculus)
5. Mgt of Coma
a. First line
i. Correct ABCs
ii. IV line
iii. Blood tests
iv. Hx from witness
v. Careful exmn, focal signs
b. 2nd line
i. ? glucose
ii. > naloxone – if narcotic od
iii. ? flumazenil – if benzo od
c. Arrange brain imaging and call ICU team

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