Neurology



Neurology






Decreased consciousness

↓consciousness occurs in many diseases requiring admission to intensive care, and is often a cause for admission in its own right. Changes in neurological state may be related to intracranial pathology, or may occur in response to respiratory, circulatory, or metabolic disorders.

The immediate management of ↓consciousness should aim to protect the airway, ensure adequate respiration, prevent BP fluctuations, and maintain adequate oxygen delivery to the brain.


Causes


Physiological derangement



  • Hypoxia.


  • Hypercapnia.


  • Hypotension.


  • Hypothermia/hyperthermia.


  • Hypoglycaemia/hyperglycaemia.


  • Other metabolic derangement (e.g. hyponatraemia/hypernatraemia, hypocalcaemia, hypermagnesaemia, hyper-osmolar states).


  • Endocrine disease (e.g. hypothyroidism/hyperthyroidism, Addison’s disease).


  • Hepatic failure, renal failure.


Intracranial damage



  • Diffuse brain injury.


  • Extradural haemorrhage, subdural haemorrhage, intracerebral bleed.


  • Stroke/ischaemia.


  • Tumour/other intracerebral mass.


  • Cerebral oedema.


Seizures



  • Status epilepticus, post-ictal states.


Infections



  • Meningitis, encephalitis, intracranial abscess.


  • Systemic sepsis.


Drugs and toxins



  • Alcohol, sedatives, illicit drugs.


Presentation and assessment

Level of consciousness should be quantified using the Glasgow coma score (GCS) or AVPU systems (rather than poorly defined terms such as unconscious, semi-conscious, obtunded, comatose).

GCS assesses eye, verbal and motor responses and has a maximum score of 15 (fully conscious) and a minimum score of 3 (deeply unconscious/comatose). A GCS <8 equates to ‘unconsciousness’ (in the AVPU scale P is taken as the cut-off).






  • Transient loss of consciousness, or changes in consciousness are also important, particularly following head injuries.


  • Obtain a contemporaneous history if possible (e.g. from patient, relatives or ambulance crew):



    • Mechanism of injury (particularly in trauma cases, image p.178)


    • Any history of headaches, amnesia, limb weakness, seizures, vomiting, slurred speech


    • Any past or current medical history


    • Any medications (especially anticoagulants) or illicit drug use


    • Previous neurosurgery

Other indicators of altered neurological state may include:



  • Drowsiness, agitation, incoherence.



  • Incontinence.


  • Headache, amnesia.


  • Vomiting.


  • Seizures.


  • Evidence of meningism (painful neck flexion or straight-leg raising—often lost if GCS ≤5) may indicate meningitis or encephalitis.


  • Evidence of head or neck trauma, especially evidence of vault or base-of-skull fracture (see image p.179).


  • Focal neurological signs and symptoms including:



    • Loss or change in sensation (anaesthesia or paraesthesia) or power


    • Gait or balance problems


    • Problems speaking or understanding speech


    • Problems reading or writing


    • Abnormal peripheral or central reflexes (including lack of gag/cough reflex)


    • Abnormal plantar responses


    • Visual changes (e.g. blurred or double vision, or loss of visual field)


  • Eye examination may reveal:



    • Pupil signs: abnormal size, difference in size, reactivity, accommodation, deviation, or movements


    • Fundoscopy (if possible): haemorrhages, papilloedema


  • Raised ICP (>20 mmHg) where monitored.

Other signs and symptoms may include:



  • Airway: grunting, snoring, or complete obstruction may occur (airway obstruction may cause, or be caused by, loss of consciousness).


  • Respiratory:



    • Hypoventilation is a late sign unless associated with narcotic/drug overdose


    • Hyperventilation and/or Kussmaul’s breathing may indicate a metabolic acidosis (e.g. DKA)


    • Cheyne-Stokes is associated with brainstem events or raised ICP


    • Tachypnoea causing a respiratory alkalosis may sometimes occur


    • Neurogenic pulmonary oedema


  • Cardiovascular changes:



    • Tachycardia or hypotension may occur if there is associated trauma (especially spinal)


    • Bradycardia is often a late or pre-terminal sign


    • Hypertension may be associated with pain or agitation, or may be associated with severe neurological injury (more likely in patients who are deeply unconscious)


    • Cushing’s response of hypertension combined with bradycardia is a late sign indicative of severe intracranial hypertension


    • ECG changes: ischaemic changes can occur in association with subarachnoid or intracerebral bleeding; cardiac ischaemic events or arrhythmias (Stokes-Adams attacks) can cause ↓consciousness; chronic AF is associated with thromboembolic events


  • Renal: incontinence, polyuria.



Investigations



  • ABGs (for hypoxia, hypercapnia, acidaemia and anion gap).


  • FBC, coagulation screen (particularly in anticoagulated patients, or where acute liver failure is possible).


  • U&Es (especially to look for hyponatraemia or AKI, LFTs, CK).


  • Serum glucose, with urinalysis for ketones if indicated (may identify hypo-, hyperglycaemia, or HHS/HONK).


  • Plasma osmolality (may help identify ethanol, methanol, or ethylene glycol poisoning).


  • Crossmatch blood (if there is trauma or risk of bleeding).


  • Blood alcohol levels and/or urine toxicology (for illicit drugs).


  • Blood, urine, and sputum cultures where infection is a possible cause.


  • ECG (tachyarrhythmia or bradyarrhythmia).


  • CXR (malignancy or pneumonia may be present).


  • Lumbar puncture (usually after CT head, see image p.574).


  • CT head (and possible also neck, see image Criteria for the request for CT scan of the head and also p.182).


  • MRI head (investigation of choice for suspected brainstem lesions).


  • In patients with associated trauma also consider: C-spine X-rays, other trauma X-rays (e.g. pelvis or long bones), skull or facial X-rays.


  • CFAM/EEG may be indicated if status epilepticus is suspected.





Further management



  • Worsening neurological state due to respiratory, cardiac, or metabolic disorders will often respond to successful management of the precipitating disorder.


Neurosurgical referral



  • Where ↓level of consciousness is suspected, or proven, to be neurosurgically treatable then referral is indicated.



Ventilation



  • Hypoxia should be avoided, as should hypo- or hypercapnia; an SaO2 >94%, PaO2 >13 kPa, and PaCO2 4.0-4.5 kPa should be maintained.



  • Pulmonary oedema may require the addition of PEEP (although caution may be required as high levels of PEEP may increase ICP).


  • Aspiration and chest infections are common in patients with ↓consciousness and should be actively sought/treated.


  • Head-up positioning may decrease the risk of aspiration and improve cerebral venous drainage.


Cardiovascular



  • Hypotension should be avoided; a MAP >90 mmHg should be sufficient initially:



    • MAP may be guided later by ICP (allowing calculation of CPP) or other measurements (see image p.186)


  • Fluid resuscitation (avoiding hypotonic fluids) is often sufficient, although inotropes may be needed.


Sedation



  • Sedation will be required in most cases where patients are intubated and ventilated.


  • Sedatives with rapid offset (e.g. propofol) are useful initially as they can be discontinued and the level of consciousness rapidly reassessed.


  • Muscle relaxants may be required initially for endotracheal intubation, or for short periods during transfer or CT scanning; however, they run the risk of masking seizure activity:



    • Where neuromuscular blockade is used consider concurrent sedative infusions with anticonvulsive prophylaxis (e.g. propofol or midazolam), or CFAM/EEG monitoring.


Metabolic



  • Hyper- or hypoglycaemia should be avoided.


  • Hyper- or hyponatraemia should be corrected (see image pp. 208 and 210).


  • Pyrexia should be avoided; the place of mild/moderate hypothermia for severe neurological injuries is unclear, but is practised by some hospitals (mild/moderate hypothermia following cardiac arrest is indicated, see guidelines, image p. 103).


Pitfalls/difficult situations

Hypoglycaemia is a common treatable cause; every patient with ↓consciousness should have a finger-prick blood sugar test.



  • Drug or alcohol use is frequently associated with other causes of diminished consciousness; a high suspicion of metabolic derangement or head injury/intracranial haemorrhage is essential in these patients.


  • Diminished consciousness is common in patients sedated in intensive care for prolonged periods, or where there has been renal or hepatic dysfunction leading to a prolonged washout period of sedative medications; a low threshold for suspecting metabolic derangement, intracranial haemorrhage/ischaemia is advisable.


  • Alcoholic and coagulopathic patients are at risk of intracranial haemorrhage even after relatively minor trauma.


  • Transfer to CT or MRI is hazardous (particularly MRI where monitoring and ventilators need to be ‘magnet compatible’); scans should only be attempted once patients are stable.



  • In some cases general surgical interventions (e.g. for major internal haemorrhage) may take precedence over investigating or treating neurological problems.




1Reprinted from The Lancet, 304, 7872, Teasdale and Jennett, ‘Assessment of coma and impaired consciousness: a practical scale’, pp. 81-84, Copyright 1974, with permission from Elsevier.


Further reading

Bateman DE. Neurological assessment of coma. J Neurol Neurosurg Psychiatry 2001; 71(SI): i13-i17.

Holzer M. Targeted temperature management for comatose survivors of cardiac arrest. N Engl J Med 2010; 363: 1256-64.

Mayer S, et al. Critical care management of increased intracranial pressure. J Intensive Care Med 2002; 17: 55-1767.

Moppett IK. Traumatic brain injury: assessment, resuscitation and early management. Br J Anaesth 2007; 99(1): 18-31.

NICE. Head injury. Triage, assessment, investigation and early management of head injury in infants, children and adults. London: NICE, 2007.

Sanap MN, et al. Neurologic complications of critical illness: Part I. Altered states of consciousness and metabolic encephalopathies. Crit Care Resusc 2002; 4(2): 119-32.

Scottish Intercollegiate Guidelines Network. Early management of patients with a head injury: a national clinical guideline. Edinburgh: Scottish Intercollegiate Guidelines Network, 2009.

Sydenham E, et al. Hypothermia for traumatic head injury (review). Cochrane Database Syst Rev 2009; 2: CD001048. DOI: 10.1002/14651858.CD001048.pub4

Varon J, et al. Therapeutic hypothermia: past, present, and future. Chest 2008; 133: 1267-74.



Seizures and status epilepticus

Seizures require intensive care management if they are prolonged, are associated with underlying disease, or cause severe physiological disturbance. Prolonged seizure activity carries a significant mortality. Any seizure lasting >5 minutes should be treated as an emergency.

A working definition of status epilepticus is: a seizure lasting >10 minutes, or repeated seizure activity without full consciousness between seizures, or failure to respond to 2 first-line treatments.


Causes



  • Hypoxia.


  • Brain injury (e.g. traumatic brain injury, intracranial tumour, haemorrhagic or ischaemic stroke, TTP).


  • Metabolic/electrolyte abnormalities (e.g. hypoglycaemia, hyperglycaemia, uraemia; sodium, calcium, or magnesium derangement).


  • Eclampsia (image p. 432).


  • Infection (e.g. meningitis, encephalitis, brain abscess).


  • Drug associated: drug withdrawal (especially alcohol), drug overdose, or illicit drug use (particularly cocaine).


  • In patients known to have epilepsy, seizures may be triggered by:



    • Head trauma, alcohol, intercurrent infection


    • Subtherapeutic blood levels of antiepileptic medications


Presentation and assessment

Seizures are most commonly generalized convulsive, with:



  • Loss of consciousness.


  • Tonic-clonic muscle movements (these may become very subtle when prolonged seizure activity leads to exhaustion).


  • Subtle eye movements (sometimes the only sign).


  • Teeth clenching, tongue biting, and/or urinary incontinence.


  • Physiological response to seizure:



    • Sweating and/or hyperthermia


    • Tachypnoea (airway obstruction may occur; hypoxia is associated airway obstruction and with prolonged fits)


    • Tachycardia and hypertension


    • Organ failure: rhabdomyolysis, AKI, DIC

Non-convulsive episodes are difficult to characterize, but may involve:



  • Impaired consciousness (defined as absence or complex seizures, and can range from lack of awareness to stupor).


  • Partial seizures: features may include focal twitching, facial tics, autonomic symptoms, and/or hallucinations (gustatory, acoustic, sensory, or visual), automatic behaviour (e.g. chewing, lip-smacking).


Investigations



  • ABGs (hypoxia, metabolic acidosis, raised lactate).


  • FBC, CRP (meningitis/encephalitis or intercurrent infection).


  • Serum glucose.


  • U&Es, LFTs, serum magnesium and calcium.


  • CK (raised after prolonged fits).



  • Urine/blood βHCG (to exclude pregnancy/eclampsia).


  • Blood and/or urine toxicology screen (for alcohol or illicit drugs).


  • Serum anticonvulsant drug levels (in patients with known epilepsy).


  • CXR (to exclude malignancy, infection, or aspiration).


  • Head CT/MRI (if seizures are prolonged, or have no obvious precipitant; or if focal neurology, papilloedema, or head injury are present).


  • Lumbar puncture (if infection is possible/likely).


  • Blood, urine, and sputum cultures (if infection is likely).


  • EEG as advised by neurologists.


Differential diagnoses



  • Any disease causing spasms (e.g. rigors, myoclonic jerks, dystonia).


  • Any disease causing syncope or agitation (see image pp.152 and 192).


  • Psychogenic seizures, also known as pseudoseizures (see image Pitfalls/difficult situations).



Further management



  • Perform a head CT if required (image p.155).


  • Ensure that a full neurological assessment has been carried out and discuss the case with a neurologist.


  • Maintain PaCO2 4.5-5 kPa, PaO2 ≥10 kPa, temperature ≤37°C, Hb ≥10 g/dl, glucose 6-10 mmol/L, serum Na 135-140 mmol/L, where possible.


  • If ICP monitoring in place, maintain ICP <20 mmHg, CPP >65 mmHg.


  • Where there is evidence of hypotension commence fluid resuscitation with inotropic support if required.


  • Other complications which may require treatment include: cerebral oedema (image p.186), neurogenic pulmonary oedema (image p.86), aspiration (image p.66), lactic acidosis (image p.204), electrolyte disturbances, rhabdomyolysis and acute renal failure (image p.268), DIC (image p.306).


Pitfalls/difficult situations



  • If seizure control is achieved reassess airway as the sedative effects of treatment may require endotracheal intubation/ventilation.


  • Many drugs lower the fit threshold (e.g. flumazenil and antipsychotics).



  • Status epilepticus is not common in epileptics; always consider other causes of seizures such as infections.


  • Psychogenic seizures may be superficially similar to convulsive status epilepticus; the diagnosis is supported by the absence of hypoxia or acidosis, and if suspected a neurology opinion should be sought.


  • Where tumour or vasculitis are present consider dexamethasone.


  • Valproate may be preferred as second-line therapy for absence states.






Fig. 5.1 Algorithm for the management of status epilepticus, SIGN (2003). Reproduced with permission from Scottish Intercollegiate Guidelines Network.





1Phenytoin equivalents (P.E.) are used for fosphenytoin: fosphenytoin 1.5 mg = phenytoin 1 mg.


Further reading

Costello DJ, et al. Treatment of acute seizures and status epilepticus. J Intensive Care Med 2007; 22: 319-47.

Meierkord H, et al. EFNS guideline on the management of status epilepticus in adults. Eur J Neurol 2010; 17: 348-55.

Maganti R, et al. Nonconvulsive status epilepticus. Epilepsy Behav 2008; 12: 572-86.

NICE. The epilepsies: the diagnosis and management of the epilepsies in adults and children in primary and secondary care. London: NICE, 2012.

Rossetti AO, et al. Management of refractory status epilepticus in adults: still more questions than answers. Lancet Neurol 2011; 10: 922-30.

Scottish Intercollegiate Guidelines Network. Diagnosis and management of epilepsy in adults. A national clinical guideline. Edinburgh: SIGN, 2003.




Stroke/thromboembolic stroke

A stroke (sometimes called a cerebrovascular accident, CVA, or occasionally a ‘brain attack’) is defined as an acute focal neurological deficit caused by cerebrovascular disease that lasts >24 hours or causes death. If the focal neurological deficit lasts <24 hours the diagnosis is a transient ischaemic attack (TIA).

Cerebral infarction is caused either by thromboembolic disorders (85%) or by haemorrhage (10% intracerebral haemorrhage, see image p.172; 5% subarachnoid haemorrhage, image p.174; subarachnoid and intracerebral haemorrhages may also be caused by head injury, see image p.178).


Causes

The incidence of stroke increases with age. Causes include: Emboli:



  • Platelet aggregates from ruptured atherosclerotic plaques.


  • Left atrial or ventricular thrombus to atrial fibrillation, poor ventricular function, or myocardial infarction.


  • Paradoxical emboli (venous emboli entering the arterial circulation via patent foramen ovale, ASD, or VSD).


  • Prosthetic heart valves; indwelling lines/prosthesis.


  • Infective endocarditis.


  • Following carotid or cardiac surgery.


  • As a complication of endovascular coiling of SAH (see image p.174).

Thrombosis:



  • Rupture of atherosclerotic lesions (risk factors for atherosclerosis include age, male sex, family history, smoking, diabetes, hypertension, and hyperlipidaemia).


  • Vasculitis.


  • Cerebral venous thrombosis (caused by hypercoagulable states like dehydration, polycythaemia, thrombocythaemia, OCP medication, protein S/C deficiency, factor V Leiden deficiency).

Other:



  • Vertebral or carotid dissection (spontaneous or post traumatic).


  • Vessel occlusion by tumour/abscess.


  • Carotid occlusion (post strangulation).


  • Systemic hypotension (e.g. post cardiac arrest).

Patients who have had TIAs are at high risk of stroke, especially if:



  • They have had 2 or more TIAs within 1 week.


  • They have an ‘ABCD’ (Age, Blood pressure, Clinical features, Duration) score of ≥4.





























    • Age ≥60


    1 point


    BP ≥140/90 mmHg


    1 point


    • Speech disturbance without weakness


    1 point


    TIA lasting 10-59 minutes


    1 point


    • Diabetes present


    1 point


    • Unilateral weakness


    2 points


    TIA lasting ≥60 minutes


    2 points




Presentation and assessment

Strokes are atraumatic, but may result in associated trauma (e.g. by causing falls). They result in rapid focal or global neurological deterioration. Other signs and symptoms may include



  • Airway: grunting, snoring or complete obstruction.


  • Respiratory: Cheyne-Stokes breathing, tachypnoea, bradypnoea (hypoventilation is a late sign):



    • Neurogenic pulmonary oedema may sometimes occur


  • Cardiovascular changes: tachycardia and/or hypertension (hypertension associated with bradycardia is a late or pre-terminal sign):



    • ECG changes: ischaemic changes can occur in association with stroke (especially subarachnoid or intracerebral bleeding); AF is associated with thromboembolic events


  • Renal: incontinence.


  • Neurological: agitation, diminished consciousness:



    • Common presentations: a commonly used system combining anatomical and clinical systems for classifying strokes is the Oxford acute stroke classification system (image p.169)


    • Atypical presentations: seizures, falls, or personality change


    • Thrombotic stroke often presents with evolving neurology, whilst embolic stroke presents with sudden onset, rapidly developing neurology


Investigations



  • ABGs (in case of hypoxia or metabolic acidosis).




  • Coagulation screen (in case of coagulopathy).


  • U&Es, LFTs, serum calcium.


  • Serum glucose (hypo/hyperglycaemia).


  • Serum lipids.


  • ECG (ischaemia, AF).


  • Head CT scan (to clarify diagnosis, extent of cerebral damage, differentiate infarct from haemorrhage and exclude hydrocephalus).


  • Carotid Doppler studies (to identify carotid stenosis of >70%).


  • ECHO (the source of any emboli may be cardiac).


  • Other investigation that may be of benefit include:





    • Thrombophilia screen


    • Auto-antibody screen


    • Plasma electrophoresis


    • Blood cultures


    • Syphilis screen


Differential diagnoses



  • Migraine.


  • Hypoglycaemia.


  • Partial epileptic seizures, or following seizures (post-ictal states).


  • Space-occupying lesions (e.g. tumour, abscess or subdural haematoma).


  • Demyelinating disease.


  • Cerebral venous thrombosis.





Further management



  • If not already performed, brain imaging should be undertaken within 24 hours where possible.


  • Ensure adequate hydration and nutrition (often NG feeding is required until a swallowing assessment can be performed).


  • Aspirin (50-300 mg) should be continued until an alternative antiplatelet therapy is started.


  • Prior statin therapy should be continued.


  • Anticoagulation is controversial; heart lesions are the only definite indication for full anticoagulation.


  • Lowering BP may extend the infarct; it is unclear at what point a high BP requires may benefit from treatment:



    • Consider using short-acting agents to reduce BP slowly if ≥220/110 mmHg


  • Ensure adequate analgesia and DVT prophylaxis.


  • Maintain blood glucose 4-10 mmol/L.


  • Investigate and treat fever aggressively (aspiration is a common cause of infection).


  • Aggressive physiotherapy and transfer to a specialist stroke unit are associated with better outcomes.


  • Consider initiating treatment aimed at modifying cardiovascular risk factors.


Pitfalls/difficult situations



  • Strokes in young patients should always raise the suspicion of ‘atypical’ causes (e.g. procoagulant disorders such as vasculitis).


  • Up to 5% of patients presenting with stroke have underlying space-occupying lesions (e.g. tumour, abscess, or subdural haematoma)


  • Where there is any history of scalp tenderness always consider temporal arteritis and measure ESR.


  • Careful BP monitoring is important following carotid endarterectomy as strokes are associated with hyper-/hypotension.


  • Haemorrhagic transformation of ischaemic strokes may occur (with or without thrombolysis).


  • Strokes after cardiac surgery or cardiac bypass present diagnostic and therapeutic challenges, especially as these patients are often extensively anticoagulated.


  • Cerebral oedema caused by a ‘malignant’ MCA territory infarct commonly occurs on day 2-5.









Fig. 5.2 Emergency management of patients with acute stroke. Adapted from NICE. Stroke: diagnosis and initial management of acute stroke and transient ischaemic attack (TIA). London: NICE, 2008.




1Reprinted from The Lancet, 337, 8756, J. Bamford et al., ‘Classification and natural history of clinically identifiable subtypes of cerebral infarction’, pp. 1521-1526.


2The final letter may be changed to denote the type of stroke: S for syndrome, I for infarct, H for haemorrhage (i.e. TACS, TACI, or TACH).


1National Institute for Health and Clinical Excellence (2008) Adapted from ‘CG 68 Stroke: diagnosis and initial management of acute stroke and transient ischaemic attack (TIA) Quick Reference Guide’. London: NICE. Available from image www.nice.org.uk. Reproduced with permission.


Further reading

AHA. Adult stroke. Circulation 2005; 112: 111-20.

Lukovits TG, et al. Critical care of patients with acute ischemic and hemorrhagic stroke: update on recent evidence and international guidelines. Chest 2011; 139: 694-700.

NICE. Stroke: diagnosis and initial management of acute stroke and transient ischaemic attack (TIA). London: NICE, 2008.

Sandset EC, et al. The angiotensin-receptor blocker candesartan for treatment of acute stroke (SCAST): a randomised, placebo-controlled, double-blind trial. Lancet 2011; 377: 741-50.

SIGN. Management of patients with stroke or TIA: assessment, investigation, immediate management and secondary prevention: a national clinical guideline. Edinburgh: SIGN, 2008.

Wardlow JM, et al. Thrombolysis for acute ischaemic stroke (review). Cochrane Database Syst Rev 2009; 4: CD000213. DOI: 10.1002/14651858.CD000213.pub2.

Vahedi K, et al. Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomised controlled trials. Lancet Neurol 2007; 6: 215-22.

van der Worp B, et al. Acute ischaemic stroke. N Engl J Med 2007; 357: 572-9.



Intracerebral haemorrhage

Spontaneous intracerebral haemorrhage (SICH) is bleeding into the parenchyma of the brain (possibly extending to the subarachnoid space). Intracerebral haemorrhage may be supratentorial or infratentorial. The associated mortality is higher than that of either thromboembolic stroke or subarachnoid haemorrhage (30-day mortality ranges from 35-52%.).


Causes



  • intracerebral haemorrhage (PICH):



    • Chronic hypertension (commonest overall cause)


    • Amyloid angiopathy


  • intracerebral haemorrhage:



    • Acute hypertension


    • Eclampsia/pre-eclampsia (image p.432)


    • Drugs: sympathomimetics and recreational drugs such as cocaine


    • Coagulopathies, especially following thrombolysis and warfarin use


    • Aneurysms and arteriovenous malformations


    • Tumours; following neurosurgery


    • Complicating CNS infections or venous sinus thrombosis


    • Haemorrhagic transformation of thromboembolic stroke.


Presentation and assessment

The presentation of intracerebral haemorrhage overlaps with that of ischaemic/thromboembolic stroke (image p.166):



  • Supratentorial haemorrhages cause sensory/motor deficits, aphasia, neglect, gaze deviation, and hemianopia.


  • Infratentorial haemorrhages cause brainstem dysfunction, cranial nerve defects, ataxia, and nystagmus.


  • The following are also common:



    • Headache, nausea, and vomiting


    • Elevated BP (up to 90% of patients)


    • Seizures (up to 10% of patients)


    • Signs and symptoms of hydrocephalus/raised ICP (image p.186).

Jun 13, 2016 | Posted by in CRITICAL CARE | Comments Off on Neurology

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