Neurological and Psychiatric Emergencies




(1)
Royal Free NHS Foundation Trust, London, UK

 




Stroke

Stroke is a clinical diagnosis, associated with an acute presentation of ongoing focal neurological deficit that cannot be explained by hypoglycaemia or other stroke mimics and which is related to a vascular cause.

Causes of acute stroke



  • Ischaemic stroke (85%)



    • Thrombotic



      • Large artery atherosclerosis: extracranial (carotid, vertebral, aortic arch); intracranial


      • Small artery(lacunar): intracranial


      • Sinovenous


    • Embolic



      • Cardiogenic: Cardio-embolism is the commonest cause of ischaemicstroke amongst the elderly.


      • Paradoxical (peripheral source with inter-atrial defect-patent foramen ovale): cryptogenic stroke


    • Haemodynamic



      • Hypotensive(e.g., watershed-type infarcts-at frontal-parietal border, gyrus angularis, putamen and insula)


      • Mechanical obstruction


      • Vascular dissection


      • Haematological



        • Polycythaemia


        • Thrombocytosis


        • Hyperviscosity syndromes


        • Hypercoagulable states


  • Haemorrhagic stroke (15%)



    • Intracerebral haemorrhage



      • hypertension


      • trauma


      • bleeding disorders: leukaemia; thrombocytopenia


      • bleeding from an arterio-venous malformation


      • berry (saccular) aneurysm rupture


      • rupture of mycotic aneurysm


      • anticoagulant therapy


      • haemorrhagic metastases


      • bleeding into a primary brain neoplasm


      • haemorrhagic infarction


      • amyloid angiopathy


      • recreational drug ingestion, e.g. cocaine, amphetamine-like compounds


      • haemorrhagic leukoencephalopathy


    • Subarachnoid haemorrhage



      • Aneurysmal rupture


      • Arteriovenous malformation


Clinical findings suggesting cardio-embolic stroke





  • Abrupt onset of symptoms


  • Previous infarctions in various arterial sites (anterior and posterior circulation), especially if separated by time


  • Other signs of systemic thromboembolism: splenic or renal infarcts; peripheral limb ischaemia


Causes of acute stroke in childhood





  • Vascular



    • Vasculitis: systemic lupus erythematosus, Kawasaki’s disease, haemolytic uremic syndrome


    • Trauma: Neck trauma with vertebral artery injury; intra-oral trauma with carotid artery injury


    • Malformations: arteriovenous malformations, aneurysms, moya moya


    • Arterial dissection (spontaneous or traumatic)


    • Tumours


  • Infections: meningitis; encephalitis; cerebral abscess; mycotic aneurysms (septic emboli)


  • ENT infections: mastoiditis, otitis media, tonsillar or retropharyngeal abscesses, sinusitis leading to venous sinus thrombosis


  • Haematological:sickle cell disease; vitamin K deficiency; coagulopathies, e.g. haemophilia; thrombophilias: deficiency of protein C, protein S, antithrombin III; polycythaemia; acute myeloid leukaemia


  • Embolic: cardio-embolic: chronic cyanotic congenital heart disease (right to left shunts), paradoxical emboli (patent foramen ovale); valvular heart disease, including endocarditis; atrial tumours; arrhythmias; cardiomyopathy



    • Fat emboli


  • Drugs: cocaine; amphetamines; oral contraceptive pill; ergot toxicity


  • Metabolic: homocystinuria; Fabry’s disease; mitochondrial encephalopathies (MELAS syndrome); organic acidurias; hyperlipidaemias


  • Neurocutaneous syndromes: neurofibromatosis; tuberous sclerosis; Sturge-Weber syndrome


Anatomical classification of stroke

Anterior circulation



  • Large vessels: internal carotid artery and its main branches-MCA and ACA; complete MCA occlusion; occlusion of lenticulo-striate branches of MCA; posterior MCA occlusion; anterior MCA occlusion; ACA occlusion


  • Small vessels: branches from the MCA and ACA

Posterior circulation



  • Large vessels: vertebral arteries, which join to form the basilar artery and its main branches, the posterior cerebral arteries: basilar artery occlusion (massive brain stem infarction; locked-in syndrome; Anton’s syndrome)


  • Small vessels: branches from all these vessels; e.g. lateral medullary syndrome (posterior inferior cerebellar artery); penetrating branches of basilar artery: pontine lacunar infarction syndrome; circumferential branches of basilar artery: midbrain infarction

Lacunar (small, deep micro-infarcts): occlusion of deep perforating arteries, which arise from both the anterior and posterior circulation, and supply the white matter of the cerebral hemispheres and brainstem.

Subclavian steal syndrome

Border zone infarcts

Lacunar infarcts: small, deep cerebral infarcts in arterial territories of lenticulostriate and thalamoperforating arteries, paramedial branches of the basilar artery and branches of the anterior choroidal artery.



  • Pure motor hemiparesis (internal capsule, pons, cerebral peduncle): contralateral hemiparesis; isolated limb paresis


  • Pure hemi-anaesthesia, involving face, arm and leg (sensory stroke) ; dysaesthetic symptoms have also been reported in the thalamic pain syndrome of Dejerine-Roussy (thalamus)


  • Ataxic hemiparesis (ipsilateral motor hemiparesis with cerebellar ataxia) (pons, internal capsule)


  • Dysarthria/clumsy hand syndrome (pons, internal capsule): dysarthria, dysphagia, contralateral facial and tongue weakness, contralateral arm and hand weakness


  • Sensorimotor stroke (thalamus): contralateral hemiparesis, hemisensory loss

Definitions:



  • Maximum deficit from a single vascular event


  • No visual field deficit


  • No new disturbance of higher cerebral function


  • No signs of brainstem disturbance


FAST recognition of anterior circulation stroke





  • Face: does one side of the face droop? ; ask the person to smile


  • Arms: is one arm weak or numb? ; ask the person to raise both arms;does one arm drift downwards?


  • Speech: is speech slurred? ask the person to repeat a simple sentence; is the sentence repeated correctly?


  • Time: if the person shows any of these symptoms, call 999 or 911


ROSIER scale for emergency stroke recognition





  • Loss of consciousness or syncope: −1


  • Seizure activity: −1


  • New acute onset (or on awakening from sleep)



    • Asymmetrical facial weakness: 1


    • Arm weakness: 1


    • Leg weakness: 1


    • Speech disturbance: 1


    • Visual field defect 1

Range: −2 to + 5


Features of anterior cerebral artery lesions

Hemispheric



  • Either: contralateral hemiparesis, lower limb > upper limb, face; contralateral grasp reflex with paratonic rigidity (gegenhalten)


  • Both: urinary incontinence; akinetic mutism; paraplegia; anarthria; apraxia of gait; corpus callosum infarction causing inter-hemispheric disconnection syndromes (split brain syndrome)-anterior (akinetic mutism), posterior (alexia without agraphia) or complete (visual disconnection); frontal release signs (glabellar, snout, sucking, rooting, grasping and palmomental reflexes)

Medial lenticulostriates



  • Either: facial weakness


  • Left: dysarthria ± motor aphasia


Features of middle cerebral artery lesions

Hemispheric



  • Either: contralateral hemiparesis, face + upper limb > lower limb weakness; contralateral hemi-sensory loss; contralateral homonymous hemianopia


  • Left (dominant):motor aphasia (anterior); receptive aphasia (posterior); global aphasia (total MCA)


  • Right (non-dominant): visuo-spatial dysfunction; hemi-spatial neglect, anosognosia, constructional apraxia

Lateral lenticulostriates



  • Either: variable lacunar syndromes


Features of posterior cerebral artery lesions

Hemispheric



  • Either: contralateral hemianopia: homonymous hemianopia; homonymous hemianopia with central or macular sparing (due to overlap of posterior and middle cerebral arteries at the occipital pole); superior quadrantic homonymous hemianopia (lingual gyrus); inferior quadrantic homonymous hemianopia; visual neglect


  • Both: cortical blindness –visual agnosia (preserved optokinetic nystagmus); memory deficits


  • Dominant: alexia without agraphia; Gerstmann syndrome (acalculia, agraphia, finger agnosia, right-left disorientation)


  • Non-dominant: prosopagnosia (difficulty in recognizing familiar faces)

Thalamo-perforators



  • Either: hypersomnolence; sensory disturbances (hemisensory loss)


Possible levels of lesion causing hemiparesis





  • Cortex: cortical dysfunction


  • Corona radiata


  • Internal capsule


  • Brain stem



    • Midbrain: ipsilateral III nerve palsy (Weber)


    • Pons: ipsilateral VI ± VII palsy (Millard-Gubler)


    • Medulla: descending spinal tract and nucleus of V nerve


Features of posterior circulation stroke





  • The 5Ds are dizziness, diplopia, dysarthria, dysphagia and dystaxia (disequilibrium), in varying combinations, with usually at least two being present simultaneously.


  • Crossed syndromes of ipsilateral cranial nerve palsy (facial involvement) and contralateral motor and/or sensory tract dysfunction (long tract signs) are highly characteristic of posterior circulation stroke, being indicative of brainstem ischaemia.

Medulla Oblongata



  • Lateral medullary syndrome (Wallenberg): ipsilateral nystagmus, Horner syndrome (descending sympathetic tract), loss of pain and temperature sensation in the face (spinal trigeminal nucleus), limb ataxia (inferior cerebellar peduncle), dysarthria, dysphagia, dysphonia (nucleus ambiguuus with vocal cord and palatal paralysis); contralateral loss of pain and temperature sensation in the trunk and limbs (spinothalamic tract) (crossed sensory loss); vertigo


  • Medial medullary syndrome (Dejerine): ipsilateral tongue weakness with slurring of speech (XII nerve palsy); contralateral hemiplegia


  • Hemi-medullary syndrome (lateral and medial medullary infarction) (Babinski-Nageotte)



    • (Babinski-Nageotte); ipsilateral limb ataxia, facial sensory loss, Horner syndrome; contralateral hemiplegia, hemi-sensory loss; vomiting, vertigo, nystagmus

Pons



  • Lateral pontine syndrome (Marie-Foix): contralateral hemiplegia and hemi-sensory loss (loss of pain and temperature); ipsilateral ataxia, VII and VIII nerve palsy


  • Inferior medial pontine syndrome (Foville): contralateral hemiplegia and weakness of lower half of face, loss of proprioception and vibration; ipsilateral ataxia (middle cerebellar peduncle) and VI nerve palsy


  • Locked-in syndrome (bilateral vertebral artery occlusion): quadriparesis (bilateral pyramidal tract lesions in the pons); loss of speech; alertness, with preserved awareness and cognition; normal sensation; bilateral facial and oropharyngeal palsy; preservation of blinking, eyelid elevation and upward gaze (III nerve intact), allowing for communication


  • Ventral pontine syndromes



    • Millard-Gubler syndrome: contralateral hemiplegia; ipsilateral VI and UMN VII nerve palsy

      Raymond syndrome: contralateral hemiplegia; ipsilateral VI nerve palsy.

Midbrain



  • Weber syndrome: ipsilateral III nerve palsy; contralateral hemiplegia


  • Benedikt syndrome: ipsilateral III nerve palsy; contralateral hemi-ataxia and chorea


  • Claude syndrome: ipsilateral III nerve palsy; contralateral upper and lower limb ataxia and tremor


  • Parinaud syndrome (superior colliculus of dorsal midbrain): bilateral vertical upward gaze palsy; convergence-retraction nystagmus; lid retraction

Rostral brainstem



  • Top of the basilar syndrome (Anton): hypersomnolence; delirium; memory loss; confusion; mutism; visual hallucinations; eyelid retraction; unawareness or denial of blindness; vertical upward and downward gaze paralysis; skew deviation of eyes


Features of cerebellar infarction





  • Early symptoms: headache, dizziness, nausea, vomiting, loss of balance


  • Signs: truncal and appendicular ataxia; nystagmus; dysarthria


  • Later signs:



    • Brain stem compression: VI nerve paresis; complete loss of lateral gaze (compression of VI nucleus and lateral gaze centre); peripheral facial paresis (compression of facial colliculus)


    • Acute hydrocephalus


Presentations of carotid artery dissection





  • Headache


  • Neck and facial pain


  • Amaurosis fugax


  • Partial ptosis with miosis (Horner’s syndrome); acute Horner syndrome with face or neck pain is due to internal carotid artery dissection until proven otherwise


  • Neck swelling


  • Pulsatile tinnitus


  • Hypogeusia


  • Focal weakness


Presentations of vertebral artery dissection





  • Severe occipital headache and posterior neck pain


  • Lateral medullary syndrome: ipsilateral facial pain and numbness (dysaesthesiae), dysarthria or hoarseness (IX, X), contralateral loss of pain and temperatures sensation in trunk and limbs; ipsilateral loss of taste (nucleus tractus solitarius), hiccups, vertigo, nausea and vomiting, diplopia or oscillopsia, dysphagia (IX, X), disequilibrium, unilateral hearing loss


  • Medial medullary syndrome: contralateral weakness or paralysis (pyramidal tract); contralateral numbness (medial lemniscus)


  • Brainstem/cerebellum: limb/truncal ataxia; nystagmus; impaired fine touch and proprioception; contralateral impaired pain and temperature sensation in limbs (spinothalamic tract)


Causes of stroke in pregnancy and puerperium

Cardiac disease



  • Paradoxical embolism


  • Peri-partum cardiomyopathy

Thrombophilias



  • Protein C or S deficiency


  • Factor V Leiden mutation

Haematological disorders



  • Thrombotic thrombocytopenic purpura


  • Disseminated intravascular coagulation

Vascular causes



  • Arterial dissection


  • Cerebral venous thrombosis

Other causes



  • Eclampsia


  • Metastatic choriocarcinoma


Stroke mimics

Stroke is a clinical diagnosis. It is important to consider the possibility of stroke mimics, for which the treatment is different. Stroke mimics are more likely to present with positive symptoms (e.g. motor, visual or somato-sensory), while stroke is associated with negative symptoms.

Toxic/metabolic (metabolic encephalopathies):



  • Hypoglycaemia: focal neurological signs, often involving the brainstem


  • Hyperglycaemia with hyperosmolar state


  • Hyponatraemia


  • Hepatic encephalopathy

CNS disease



  • Space occupying lesion:brain tumours (primary or metastatic)-often associated with haemorrhage into tumour, rapid onset of oedema, or obstructive hydrocephalus, compression of the intracerebral microcirculation resulting in ischaemia, post-ictal weakness associated with a seizure; chronic subdural haematoma; arteriovenous malformation; cerebral abscess


  • Seizure: Post-ictal state after unwitnessed or unrecognised stroke (Todd’s paralysis-usually hemiparesis; hemi-sensory deficit); partial seizures


  • Syncope


  • Cerebral vasculitis


  • Infection: meningitis; encephalitis; cerebral abscess: rapidly progressive localized intracerebral mass lesion; non-specific signs and symptoms of raised intracranial pressure; focal neurological deficit


  • Migraine: complicated migraine (hemiplegic migraine); migraine with aura; aura without headache


  • Acute demyelinating disorders: multiple sclerosis (initial diagnosis or acute exacerbation)


  • Functional hemiparesis: conversion disorder


  • Old stroke with intercurrent illness


  • Transient global amnesia


  • Reversible cerebral vasoconstriction syndrome; posterior reversible encephalopathy syndrome


  • Acute peripheral polyneuropathy (Guillain-Barre syndrome; Miller-Fisher variant)

Stroke mimics should be considered in the presence of:



  • Reduced level of consciousness


  • Gradual onset of symptoms


  • Fever


  • Absence of focal signs


  • Fluctuating signs

Stroke chameleons represent atypical manifestations of stroke, which may lead to non-recognition:



  • Acute dyskinesias, such as hemiballismus


  • Acute confusional states (non-dominant anterior circulation strokes involving the temporo-parietal region)


  • Abnormal sensations or loss of sensation (parietal cortical and thalamic strokes)


  • Cortical blindness, with normal pupillary light reactions and normal optic disks on funduscopy


Transient ischaemic attack mimics

(causes of transient neurological symptoms)

These are important to consider and recognize where possible, given that up to 60% of patients attending TIA clinics turn out not to have a transient ischaemic attack



  • Seizure with or without Todd’s paralysis


  • Migraine aura; complicated migraine; Bickerstaff migraine (bilateral visual disturbance-visual field deficits, scintillating scotomata), dysarthria, perioral numbness, loss of consciousness


  • Hypoglycaemia


  • Space occupying lesions


  • Acute vestibular syndrome (labyrinthine disorders)


  • Syncope


  • Transient global amnesia: temporary loss of anterograde memory loss


  • Amyloid spells (cerebral amyloid angiopathy): stereotyped transient positive (aura-like spreading paraesthesiae, positive visual phenomena or limb jerking) and negative (TIA-like limb weakness, numbness, dysphasia or visual loss) symptoms


  • Paroxysmal symptoms due to demyelination: multiple sclerosis


  • Subclavian steal


Causes of transient ischaemic attack





  • Large artery atherosclerosis: carotid stenosis, vertebro-basilar disease, aortic atherosclerosis


  • Cardio-aortic embolism: atrial fibrillation, left ventricle thrombus, valvular disease


  • Small artery occlusion: intracranial small vessel disease from hypertension, increased age


  • Cryptogenic


Features which do not support the diagnosis of transient ischaemic attack (TIA mimics)





  • Alteration or transient loss of consciousness (syncope)


  • Positive symptoms


  • Generalised weakness


  • Isolated dizziness/vertigo


  • Confusion


  • Urine incontinence


  • Loss of balance


  • Amnesia


  • Falls


  • Isolated diplopia


  • Isolated dysphagia


  • Drop attacks


  • Sensory symptoms in part of one limb or in the face


Features of transient ischaemic attacks

Seventy-five percent last less than 1 h

Carotid artery territory



  • Unilateral hemiparesis


  • Unilateral hemi-sensory loss


  • Unilateral visual disturbance: homonymous hemianopia; blindness (amaurosis fugax)


  • Aphasia; dysphasia

Vertebral artery territory



  • Bilateral motor/sensory loss


  • Bilateral visual loss


  • Ataxia


  • Combinations of vertigo, diplopia, dysphagia, dysarthria


Risk stratification for TIA

ABCD2 score



  • Age >60: 1


  • Blood pressure >140/90 mm Hg: 1


  • Clinical features



    • Unilateral weakness 2


    • Speech deficit 1


  • Duration of symptoms



    • 10–59 min: 1


    • >59 min: 2


  • Diabetes mellitus: 1


Cardio-embolism

High risk sources



  • Mechanical prosthetic valves


  • Mitral stenosis with atrial fibrillation


  • Atrial fibrillation (other than lone AF)


  • Left atrial/atrial appendage thrombus


  • Dilated cardiomyopathy


  • Akinetic left ventricular segment


  • Atrial myxoma


  • Infective endocarditis

Medium risk sources



  • Mitral valve prolapse


  • Mitral annulus calcification


  • Mitral stenosis without atrial fibrillation


  • Left atrial turbulence


  • Atrial septal aneurysm


  • Patent foramen ovale


  • Atrial flutter


  • Lone atrial fibrillation


  • Bio-prosthetic cardiac valve


  • Non-bacterial thrombotic endocarditis


  • Congestive heart failure


  • Hypokinetic left ventricular segment


  • Myocardial infarction (from 4 weeks to 6 months)


Coma evaluation

Coma refers to a Glasgow Coma Score of 8 or under. ABCDE evaluation comes first

General



  • Skin: rash; jaundice; track marks


  • Temperature: fever, hypothermia


  • Blood pressure


  • Odour on breath


  • Cardiovascular: arrhythmia


  • Abdomen: organomegaly

Neurological assessment



  • Meningeal signs


  • Funduscopy: papilloedema; subhyaloid haemorrhages; hypertensive retinopathy; diabetic retinopathy


  • Tympanic membranes


  • Brain stem function:



    • Pupillary reactions: size, symmetry, light reaction


    • Spontaneous eye movements


    • Oculocephalic (doll’s eye) responses


    • Oculovestibular (caloric) responses


    • Corneal responses


    • Abnormal eye positions: dysconjugate gaze; skew deviation (vertical separation of ocular axes); tonic deviation


    • Gag responses


  • Respiratory pattern



    • Cheyne-Stokes breathing: alternating hyperventilation and apnoea


    • Central neurogenic hyperventilation: rapid, regular, deep


    • Apneustic: rapid, with sudden pauses of inspiration, lasting 2–3 s


    • Ataxic: irregular unpredictable and chaotic


  • Motor function in limbs



    • Spontaneous and stimulus-induced movements


    • Tone; clonus


    • Deep tendon reflexes; plantar responses


    • Posturing: decorticate (bilateral upper limb flexion and lower limb extension); decerebrate (bilateral upper and lower limb extension)


Clinical categorisation of coma





  • No focal or meningeal signs: toxic-metabolic encephalopathy (normal pupils (except with opiates); multi-focal myoclonus)


  • Meningeal signs; no focal signs: subarachnoid haemorrhage; meningitis; meningoencephalitis


  • Focal signs: intracranial haemorrhage, space occupying lesion (tumour; abscess; infarction)


Pupillary signs in coma





  • Enlarged and reactive: sympathomimetic intoxication (amphetamines, cocaine)


  • Fixed and dilated: anticholinergic intoxication


  • Mid-position and unreactive: focal midbrain dysfunction, related to enlarging supratentorial space-occupying lesion


  • Constricted: opioid intoxication


  • Unilateral dilated: ipsilateral IIIrd nerve compression caused by uncal herniation


Mnemonic for causes of coma





  • A: alcohol; acidosis


  • E: epilepsy; electrolyte; encephalopathy; endocrine


  • I: insulin


  • O: opium; oxygen (hypoxia)


  • U: uraemia (metabolic)


  • T: trauma; tumour; temperature


  • I: infection (CNS or other)


  • P: psychiatric; poisoning


  • S: shock; space occupying lesion; stroke


Causes of coma

Supra-tentorial structural lesions:

Mass lesion with tentorial herniation; bilateral hemisphere damage; bilateral thalamic lesion (asymmetrical neurological deficits of movement, posturing reflexes, and gaze; dilated fixed pupil; partial or secondarily generalized seizures)



  • Subarachnoid haemorrhage


  • Extradural haematoma


  • Subdural haematoma


  • Tumour


  • Intracranial haemorrhage


  • Infarct


  • Abscess


  • Venous sinus thrombosis


  • Head injury


  • Infra-tentorial structural lesions

Brain stem compression (posterior cranial fossa lesion) or primary brain stem disease (basilar artery thrombosis) (early development of quadriparesis; cranial nerve palsies; loss of brain stem reflexes; apnoea)



  • Infarct


  • Haemorrhage


  • Tumour


  • Inflammatory lesion

Diffuse (bilateral hemispheric dysfunction) (preserved pupillary light reflexes; nystagmus; myoclonic jerks; tremor; bilateral asterixis; primary generalized seizures)



  • Metabolic encephalopathy: hypoglycaemia; hyperglycaemia; hyponatraemia; hypernatraemia; hypercalcaemia; hypocalcaemia


  • Hypoxia; hypercapnia


  • Acidosis


  • Hepatic encephalopathy


  • Uraemia


  • Adrenocortical failure


  • Inborn errors of metabolism: organic acidurias and organic acidaemias,


  • Urea cycle defects, mitochondrial and carnitine disorders, fatty acid


  • Oxidation defects, leukodystrophies


  • Toxic: ethanol; methanol


  • Drug overdose: sedative-hypnotics (benzodiazepines); opiates; tricyclic antidepressants


  • Epilepsy: non-convulsive status epilepticus (nystagmoid jerks of eyes, myoclonic limb movements, akathisia)


  • Environmental: hypothermia; heat stroke; carbon monoxide


  • Infections


  • Meningitis


  • Encephalitis


Features suggestive of metabolic encephalopathy





  • Delirium


  • Fluctuating level of consciousness


  • Motor phenomena: tremor; asterixis; multi-focal myoclonus


  • Hallucinations


  • Impaired remote memory


  • Sparing of pupillary reactions


  • Normal ocular movements


Differential diagnosis of coma (coma mimics)





  • Akinetic mutism


  • Locked-in syndrome: alert and awake; unable to communicate except through blinking and vertical eye movements; quadriplegia with all other voluntary movements abolished, including those depending on innervation by lower cranial nerves; due to destructive lesions of the basis pontis interrupting the corticospinal and corticobulbar pathways, with sparing of auditory tracts and ascending sensory tracts


  • Persistent vegetative state: loss of cognitive function, retained automatically controlled visceral functions, papillary reflexes, and reflex postural responses to noxious stimuli


  • Generalised muscle paralysis due to neuromuscular blocking drugs or an acute neuromuscular disease


  • Catatonia: rigidity, mutism, unresponsiveness to environmental stimuli, eyes open; optokinetic and vestibulo-ocular responses maintained; waxy flexibility, catalepsy, posturing and grimacing


  • Abulia: severe apathy


Mimics of brain death

(coma with absent brain stem reflexes and apnoea, after exclusion of reversible confounders)



  • Severe metabolic disease with potentially reversible coma


  • High spinal cord injury


  • Peripheral nerve or muscle dysfunction or neuromuscular blockade accounting for unresponsiveness: Guillain Barre syndrome


  • Organophosphate/baclofen toxicity


  • Profound hypothermia


Features of psychogenic coma





  • Normal physical examination


  • Symmetrical reduced tone


  • Normal symmetrical reflexes


  • Flexor plantar responses


  • Nystagmus with ice water calorics


Causes of reduced level of consciousness in children





  • Shock (hypovolaemic, distributive-anaphylactic, cardiogenic)


  • Sepsis


  • Metabolic diseases


  • Intracranial infection


  • Raised intracranial pressure


  • Convulsions; post-ictal


  • Intoxication (alcohol), poisoning


  • Trauma (blood loss; traumatic pneumothorax; cardiac tamponade)


  • Stroke


  • Hypertensive encephalopathy


  • Acute hydrocephalus


Glasgow Coma Score

Eye opening

4: Spontaneous eye opening

3: Eye opening to verbal command

2: Eye opening to pain

1: None

Best verbal response

5: Orientated

4: Confused conversation

3: Inappropriate words

2: Incomprehensible sounds (moaning, groaning)

1: None

Best motor response

6: Obeys commands

5: Localizes pain (movement localized to painful stimulus)

4: Withdraws from pain

3: Abnormal flexion to pain (decorticate posturing) (upper limb adduction; flexion of arms, wrists and fingers; extension and internal rotation of lower limbs, plantar flexion of ankles)

2: Extension to pain (decerebrate posturing) (upper limb adduction;extension of legs; plantar flexion of ankles)

1: None


Problems with use of the Glasgow Coma Score





  • Inter-rater variability


  • Confounding factors



    • Eye opening: swelling of eyelids (ocular or facial trauma); IIIrd nerve palsy


    • Best verbal response: dysphasia/aphasia; sedation; tracheal intubation/tracheostomy; dementia; alcohol or drug intoxication; tongue oedema; fractures of mandible/maxillae; language difficulty; psychiatric disease; mutism


    • Best motor response: neuromuscular blockade; spinal cord/brachial plexus injury; splints/immobilization devices


Seizure characteristics





  • Paroxysmal episodes


  • Abrupt onset


  • Self limited


  • Stereotyped


  • Lateral tongue bite is pathognomic; bites of the tip of the tongue can be associated with syncope


  • Post-ictal confusion/sleep


Seizure presentations





  • Generalised convulsive movements


  • Transient loss of consciousness


  • Transient focal motor or sensory attacks


  • Facial muscle and eye movements


  • Episodic phenomena during sleep


  • Prolonged confusional state


  • Automatisms


  • Psychic experiences


  • Aggressive or vocal outbursts


Features of generalized tonic-clonic seizures





  • Vocalisation at the onset


  • Tonic phase (10–30 s) with apnoea, cyanosis, hypersalivation, urine and faecal incontinence, mydriasis and upward eye deviation


  • Clonic phase (30–60 s)


  • Typically, last less than 1 min


Features of complex partial seizures





  • Formed hallucinations: visual; auditory; gustatory; olfactory


  • Dyscognitive experiences: depersonalization; dreamy states: déjà vu; jamais vu


  • Affective states: fear, depression, elation


  • Automatisms (ictal and post-ictal repetitive non-purposeful behaviour): lip smacking, chewing, repeating words or phrases


  • Transient amnesia


  • Typically, last less than 3 min


Features of absence seizures





  • Brief discontinuation of activity


  • Unresponsiveness, unawareness and subsequent lack of recall


  • Associated features (with complex absence seizures) include clonic movements (blinking of eyelids, nystagmus, limb jerking), changes in tone (reduced or decreased), subtle automatisms (oral, vocal or gestural), and autonomic features (changes in skin colour, mydriasis, urine incontinence)


Features of occipital lobe seizures





  • Visual symptoms: positive (light flashes, colours) or negative (scotomas, field defects) phenomena


  • Complex visual phenomena, e.g. hallucinations (relatively uncommon)


Causes of symptomatic (provoked) seizures





  • Acute metabolic disturbance: hypoglycaemia; hyperglycaemia; hyperosmolar state; hyponatraemia, hypocalcaemia, hypomagnesaemia


  • Acute/subacute neurological disorders: CNS infection; mass lesion/vascular malformation; stroke (cerebral haemorrhage); subarachnoid haemorrhage; HIV encephalopathy; hypertensive encephalopathy


  • Medication toxicity


  • Alcohol or drug (heroin, cocaine, amphetamine, methadone) overdose or withdrawal


  • Head injury


  • Hyperthermia; febrile convulsion


Seizure mimics





  • Convulsive syncope


  • Migraine


  • Sleep disorders


  • Conversion disorder


  • Paroxysmal cardiac arrhythmia


  • Breath-holding spells

The diagnosis of epilepsy should only be made by a neurologist with training and expertise in epilepsy as misdiagnosis is common.

The International League Against Epilepsy (ILAE) task force for the diagnosis of epilepsy includes:



  • At least two unprovoked (or reflex) seizures occurring more than 24 h apart, or


  • One unprovoked (or reflex) seizure and capability of further seizures similar to the general recurrence risk after two unprovoked seizures (at least 60% over the next 10 years), or


  • The diagnosis of an epilepsy syndrome


International Classification of Epileptic Seizures

Focal (or partial)



  • Simple partial (no loss of consciousness)


  • Complex partial (with impaired consciousness at the onset, or simple partial onset followed by impaired consciousness)


  • Complex partial seizure evolving to generalized tonic-clonic seizure

Generalised (convulsive or non-convulsive with bilateral discharge involving sub-cortical structures): absence, myoclonic, clonic, tonic, tonic-clonic, atonic

Unclassified


Features of generalized genetic epilepsies





  • Childhood or teenage onset; onset above the age of 25 years is unusual


  • Triggered by sleep deprivation or alcohol


  • Early morning tonic-clonic seizures or myoclonic jerks


  • Short absence seizures


Features of simple febrile seizure





  • Child aged 6 months to 5 years


  • Generalised clonic or tonic-clonic seizure, lasting less than 15 min


  • No neurological abnormality by examination or by developmental history


  • No recurrence within the following 24 h


  • Fever and seizure not caused by meningitis, encephalitis, or other brain illness


Features of complex febrile seizures





  • Lasts longer than 15 min


  • Focal seizure, with or without secondary generalisation


  • Todd’s paralysis may be present


  • Repetitive seizures may occur


Features suggestive of CNS infection causing seizure



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Nov 20, 2017 | Posted by in Uncategorized | Comments Off on Neurological and Psychiatric Emergencies

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