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Neurology: overview

Neurology is a fascinating specialty with increasingly sophisticated tools of diagnosis and a range of therapies for diseases affecting the brain and nerves. It is clinically wide ranging, from acute inpatient stroke services to outpatient clinics managing chronic degenerative conditions such as Alzheimer’s and Parkinson’s diseases.

Cases to see


Attend headache clinics to differentiate between primary headache syndromes and headaches secondary to alternative diagnoses and note the subtle differences between numerous primary headache syndromes.


Common outpatient referrals for ‘fits’ and ‘funny turns’, observe how important history is in diagnosing epilepsy or, frequently, its many mimics. Observe how choosing treatment options is a fine balance between benefits in reducing seizures while minimizing side effects; be aware of how a diagnosis of epilepsy can change a patient’s life, e.g. ability to drive.

Parkinson’s disease and movement disorders

Frequently encountered among older inpatients as a comorbidity, managed in outpatients either by geriatricians or neurologists. Try to see complex patients with limitations of maximal treatments, treatment complications, significant non-motor symptoms, and assessments of neurosurgical treatment options such as deep brain stimulation.

Dementia and memory

Cognitive impairment secondary to Alzheimer’s disease, vascular causes, or Lewy body disease is commonly encountered among older inpatients and outpatient memory clinics. Attend tertiary centre dementia clinics for typically younger and atypical patients with more unusual causes of cognitive impairment, such as frontotemporal dementia, CJD, and corticobasal degeneration.

Motor neuron disease

Typically encountered in specialist outpatient clinics. Try to obtain a grasp of neurophysiological testing in diagnosis. Be aware of the multidisciplinary input required including palliative care physicians, dieticians, and potentially respiratory and gastroenterological inputs as this degenerative condition progresses.

Emergency cases


Shadow the stroke registrar on call to attend thrombolysis calls for patients presenting within 4.5 hours of symptoms starting and watch a National Institutes of Health Stroke Scale (NIHSS) international) examination, then follow the patient through their hyperacute neuroimaging.

On acute wards, the emphasis changes to finding the underlying cause of stroke and preventing further events while a MDT begins intensive rehabilitation.

Guillain–Barré syndrome

Potentially rapidly progressive, frequently encountered as an emergency on the acute medical take; urgent cardiac monitoring, spirometry, and swallowing assessments are required. Relatively stable patients can be found receiving IV immunoglobulin on the neurology ward while more unwell patients may require intubation on the ICU.


Frequently a differential diagnosis on the acute medical take; good opportunity to watch a lumbar puncture and familiarize yourself with local hospital policies on CNS infections

Myasthenia gravis

Familiarize yourself with the emergency investigations when encountering a patient with fatiguable muscle weakness: is their respiratory function compromised? Can they swallow? If the diagnosis was previously known, are there metabolic or infectious causes for this patient’s decompensation?

Idiopathic intracranial hypertension

A good opportunity to practise fundoscopy and see swollen optic discs; often another good opportunity to observe a LP.

Procedures to see

Lumbar puncture

Performed on either the ward or outpatient day-case unit, LPs are performed aseptically using local anaesthetic. The needle passes between the spinous processes at L3/L4, anatomically defined as the intersection of two iliac crests. The opening pressure is measured and samples collected for cell count, protein, glucose, and other specialized tests such oligoclonal bands helpful in the diagnosis of MS. Before the back is cleaned, make sure you ask the doctor and patient to feel the anatomical landmarks.

Nerve conduction studies

Neurophysiologists test peripheral nerve conduction by passing electricity via needle electrodes through two points of a nerve, calculating conduction velocity and signal amplitude, the pattern of which helps to determine the underlying cause of a neuropathy. Loss of the myelin coating causes a reduction in conduction velocity; axonal loss reduces amplitude in the presence of conduction block across a defined segment.

Electroencephalography (EEG)

Scalp electrodes can be used to record brain electrical activity. One of the main uses is to find seizure activity suggestive of epilepsy.

Abnormalities may be found in between seizures (‘interictal abnormalities’). Activation procedures such as hyperventilation, photic stimulation (strobe lighting), or sleep deprivation may be used to enhance subtle abnormalities. Patients may be admitted for a prolonged period of EEG recording while under close observation (video telemetry), allowing observed attacks to be correlated with the EEG. This is helpful in identifying a focus that may be triggering seizures, which can be a target for surgical resection, or for diagnosing non-epileptic attacks. Find your nearest neurophysiology department and arrange to attend for a couple of hours to see some of these procedures being performed.

Things to do

The majority of learning comes from taking as many focused histories and examining as many neurological patients as possible. Most departments have regular neuroradiology MDT meetings (see Fig. 22.1), where radiologists point out significant and interesting features on CT and MRI scans. Neurosurgical MDTs can be useful to see the overlap between medical and surgical treatments in difficult to manage patients with epilepsy and Parkinson’s disease. Shadow the stroke registrar to encounter how speed can make all the difference in a thrombolysis call and attend the stroke MDT to experience how a multidisciplinary setting helps patients with neurological deficits improve their mobility and cope at home.

Neurology: in clinic

Idiopathic intracranial hypertension

A condition of uncertain aetiology in which intracranial pressure is raised (>25 cm water), not secondary to a space-occupying lesion or other ‘physical’ causes such as venous sinus thrombosis.


It is most common in young, overweight women, and the main symptom is headache, typically worse on lying flat, coughing, or straining. Visual symptoms include blurring, field loss, and fleeting blackouts of vision, and if untreated, the major risk is visual loss.


Patients may be admitted for lumbar puncture, which measures the pressure and provides temporary relief as CSF is removed. Perform fundoscopy as many will have papilloedema, and examine eye movements as sixth nerve palsies can occur as a false sign of raised pressure.


Is with weight loss, and acetazolamide to reduce CSF production. If vision is threatened, surgery (LP CSF shunting) is required.

Parkinson’s disease

‘Parkinsonism’ describes the combination of bradykinesia, rigidity, resting tremor, and postural instability, of which the most common cause is idiopathic Parkinson’s disease, caused primarily by degeneration of nigrostriatal dopaminergic neurons in the basal ganglia. Idiopathic Parkinson’s disease can also present with non-motor features such as postural instability, bladder and bowel dysfunction, and cognitive impairment, ranging from mild to dementia.


Conditions mimicking idiopathic Parkinson’s disease include vascular disease, encephalitis, and drug-induced Parkinsonism, classically by MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), used by 1980s Californian meperidine addicts.

Parkinson’s plus syndromes

Display atypical Parkinsonism features such as lack of asymmetry, anosmia, and poor response to levodopa, as well as their individual characteristic symptoms, and you should learn one or two distinct features of multisystem atrophy, progressive supranuclear palsies, and corticobasal degeneration. It is a safe bet to be asked about dopamine metabolism, levodopa precursors, and monoamine oxidases in clinic when you are discussing drug treatments which target this pathway.


As affected dopaminergic neurons continue to degenerate, patients often become resistant to therapy after 5 years, and develop new involuntary movements: levodopa induced dyskinesias and increasing psychiatric features.


See Fig. 22.2.

Fig. 22.2 Parkinson’s medical treatment.

Fig. 22.2 Parkinson’s medical treatment.

Reproduced from Rogers et al. Parkinson’s disease: summary of updated NICE guidance. BMJ 2017;358:j1951.


It is important to distinguish between primary headache (no underlying pathology, e.g. migraine, tension and cluster headaches) and headaches secondary to other conditions (underlying pathology, e.g. infectious, neoplastic, vascular or drug induced. 10–15% of ED attendances with headache have a serious underlying cause). See Table 22.1 for subtypes and features.

Table 22.1 Subtypes of headache











Unilateral around temple

Hours–3 days




Photophobia, N&V, visual disturbance



Whole head

30 min–1 week



Tight pressure around head

Sore shoulders




30 min–2 hours

1–8 times/day/at night



Unilateral tearing, nasal congestion



Neck base

1–6 hours



Dull to severe

Neck pain, nausea

Red flags

For secondary headaches: new/change in headache in patients >50 years; sudden-onset ‘thunderclap’ headache; neurological symptoms; headache that changes with posture, wakes the patient, or is precipitated by physical exertion; jaw claudication; visual disturbance; neck stiffness; fever; and history of cancer/HIV.


All patients should have their BP checked and a neurological exam including fundoscopy. Investigation is rarely needed for primary headaches. Perform CT on those with a first presentation of thunderclap headache (98% sensitive for SAH at 12 hours, dropping to 93% sensitive at 24 hours). Consider LP looking for xanthochromia at 12 hours post onset if CT negative. This can be positive for up to 2 weeks. Perform ESR and CRP if giant cell arteritis (GCA) is suspected.


  • Try simple analgesia first: paracetamol and NSAIDS (aspirin/ibuprofen/naproxen). Avoid opioids.

  • Antiemetics (prochlorperazine/domperidone/metoclopramide) and 5HT1 receptor antagonist (e.g. sumatriptan) for migraines.

  • Beta blockers (propranolol) or TCA (amitriptyline) can be used for migraine prophylaxis.

  • Give high-flow oxygen for cluster headache.

  • Provide high-dose prednisolone for GCA.

  • Advise stress management, adequate hydration, good sleep hygiene, minimal TV/PC screen time, and review by the optician.


Are by far the most common primary headache, classically unilateral, pulsating headaches lasting between 4–72 hours, exacerbated by movement, and associated with nausea, photophobia, and phonophobia, and needing to lie in a dark room. Family history of migraines is common. Patients are asked about preceding symptoms such as flickering lights in the hour before the headache (the aura).


Acute attacks are treated with NSAIDs and antiemetics, before escalation to specific antimigraine drugs such as triptans. Frequency of migrainous attacks are reduced with beta blockers (e.g. propranolol) and anticonvulsants (e.g. sodium valproate).

Multiple sclerosis

MS is an autoimmune disease resulting in the inflammation and damage of myelin sheaths around the white matter of the CNS.


It classically affects women in their 30s and can present with a variety of symptoms depending on the area affected: weakness, loss of sensation, paraesthesia, and visual disturbances can all present.


Read about the McDonald diagnostic criteria, which aim to establish two or more episodes of CNS inflammation separated in time and location. MRI brain and spine can be helpful in detecting small areas of inflammation or old plaques; detection of oligoclonal bands in CSF but not in serum is suggestive of CNS inflammation and supportive of MS as a diagnosis.


Of MS is highly variable between patients and you will better understand this after spending half a day in an MS clinic, where you will also learn about MDT management which also seeks to better address the patient’s symptoms. The disease can continue to deteriorate (primary progressive) or progress in relapsing/remitting pattern with episodes of recovery.


Steroids are used to reduce the length of symptoms in acute relapses but only DMARDs affect progression (e.g. interferon beta).

Motor neuron disease

A progressive degenerative disease of upper and lower motor neurons, frequently presenting as asymmetric bilateral limb weakness, dysphagia, dysarthria, and dyspnoea (eventually Neurology possible respiratory failure). See Table 22.2 for subtypes.

Table 22.2 Motor neuron disease subtypes


Upper motor neuron degeneration

Lower motor neuron degeneration

Progressive muscular atrophy (PMA)



Progressive bulbar palsy (PBP)



(bulbar region)

Primary lateral sclerosis (PLS)



Amyotrophic lateral sclerosis (ALS)



Clinical examination

Typically demonstrate a combination of lower motor neuron signs such as muscle wasting and muscle and tongue fasciculations; and upper motor neuron signs such as brisk reflexes and upgoing plantars. There is no single diagnostic test and treatment is symptom control. Disease subtypes are shown in Table 22.2.

Myasthenia gravis

An autoimmune disorder in which antibodies attack nicotinic acetylcholine receptors of the neuromuscular junction.


The hallmark is muscle weakness with fatiguability on exertion which makes for some interesting examination techniques to elicit this feature. Muscles commonly affected are those of the eyes, speech and swallowing, neck, proximal limbs, and respiration (most dangerous).


In the history ask in particular about fatiguability or fluctuation of symptoms (e.g. may be worse in the evening).


You should examine these patients for ptosis, which may be brought out with sustained upgaze, complex ophthalmoplegia which does not fit the pattern of a particular cranial nerve, and fatiguable weakness of the neck and limbs.


Is by identification of the antibodies and by neurophysiological studies.


During acute episodes, patients may receive IV immunoglobulin or plasma exchange. Symptomatic treatment is with pyridostigmine, a cholinesterase inhibitor, with the mainstay of treatment by immunosuppression. Some patients have an abnormality of the thymus and may respond to thymectomy.

Peripheral neuropathy

To understand peripheral nerve disorders it is important to have a good knowledge of anatomy. Make sure you know which nerves and nerve roots supply the major muscles, and the sensory coverage of the dermatomes and major peripheral nerves (median, radial, ulnar, and common peroneal).


Means dysfunction of a single peripheral nerve, and is usually due to compression, e.g. carpal tunnel syndrome affecting the median nerve.

Mononeuritis multiplex

Means dysfunction of multiple named peripheral nerves (e.g. median and common peroneal), and can result from multiple sites of compression or systemic vasculitis. Generally, however, the term peripheral neuropathy is taken to mean a condition of damage to all peripheral nerves (polyneuropathy). Usually the longest nerve fibres are worst affected, giving a characteristic pattern of distal weakness and 'glove and stocking' sensory loss. There is a long list of causes including diabetes, alcohol, vitamin B12 deficiency, and certain drugs. Inflammatory causes such as Guillain–Barré syndrome (and its chronic counterpart, chronic inflammatory demyelinating polyradiculoneuropathy) are important causes as they can be treated with immune-modulating drugs. Patients with peripheral neuropathy are often admitted for investigations such as LP and nerve conduction studies, or for treatments such as IV immunoglobulin—so use the chance to take a careful history and perform a full examination. Expect to find all lower motor neuron signs, and look closely for wasting and fasciculations which can easily be missed. Try to determine the pattern of nerve damage. Is it motor, sensory, or both?

Does the sensory component involve small fibres (pain and temperature), large fibres (proprioception and vibration), or both? Are autonomic nerves involved (check postural BP)?

Confusion: delirium and dementia

You should know the difference between delirium and dementia.


A form of organic brain syndrome characterized by:

  • disturbed conscious level (overactivity, excitement, drowsiness, stupor)

  • global disturbance of cognition (memory, orientation, attention, speech, motor function)

  • rapid onset with fluctuating course (often worse at night) and brief duration.

Delirium can occur at any age, but is more common in the elderly.


Infections (UTI, pneumonia), medications (digoxin, steroids, diuretics), withdrawal (alcohol, opioids), metabolic (hypoxia, hypercapnia, hypoglycaemia, hyponatraemia), cardiac (acute MI, cardiac failure), neurological (head injury, chronic subdural, post-ictal), organ failure (respiratory, renal, hepatic), endocrine (DM, thyrotoxicosis).



An acquired, progressive decline in intellect, behaviour, and personality. It is irreversible and typically occurs with a normal level of consciousness. Note that patients with dementia are at risk of delirium resulting from an acute infective or metabolic origin.


Patients with progressive deficits in two or more cognitive domains affecting the patient’s daily life. See Table 22.3 for subtypes.

Table 22.3 Types of dementia








Gradually progressive

  • Rapid amnesia

  • Language deficits

  • Early normal neuro and gait exam

  • Affective/behavioural symptoms

  • Brain atrophy

  • Beta amyloid plaques



Abrupt with stepwise decline

  • Focal neuro signs

  • Associated vascular disease

  • CVA

  • Lacunar infarcts

  • Brain atrophy

  • Ischaemic changes

Lewy body


Insidious onset

  • Visual hallucinations

  • Shuffling gait

  • Parkinsonism

  • Neuroleptic sensitivity

  • Generalized brain atrophy

  • Lewy body in cortex and midbrain



Insidious onset but rapid progression

  • Disinhibition

  • Socially inappropriate

  • Apathy

  • Poor executive function

  • Frontal and temporal atrophy

  • Pick cells/bodies in cortex


The most common causes are Alzheimer’s disease, Lewy body dementia, vascular dementia, and frontotemporal dementia. It is worth being aware of the existence of some of the rarer types, but more detailed knowledge of these four should suffice.

Reversible causes

Where dementias are by definition progressive and irreversible, it is essential to exclude a number of reversible mimics resulting in cognitive deficits: depression, vitamin B12 deficiency, normal pressure hydrocephalus, intracranial haematomas and masses, HIV, neurosyphilis, and hypothyroidism are importantly all reversible or treatable.

Other types include mixed dementia, CJD, Huntington's disease, and Wernicke–Korsakoff syndrome.

Alzheimer’s disease

Accounts for 70% of dementias affecting nearly half a million people in the UK, characterized by the formation of amyloid proteins and neurofibrillary tangles in the cerebral hemispheres.

Clinical features

Are characterized by the 6 A’s:

  • Amnesia (impaired formation of short-term memory).

  • Apraxia (impaired ability to perform tasks).

  • Agnosia (impaired recognition).

  • Alexia (inability to read).

  • Acalculia (inability to perform simple arithmetic).

  • Aphasia (impaired understanding and word production).

  • Visuospatial deficits can also become prominent in later disease.

Vascular dementia

Is the second commonest type and affects patients differently depending on the site of brain ischaemia. Yet it often progresses in a step-like fashion whereby symptoms may remain at a constant level for some time and the illness progresses in obvious steps rather than a gradual reduction in skills/abilities as with Alzheimer's disease. Life span is also shorter most likely due to CVS risk factors.

Frontotemporal dementia/frontal lobe dementia

Is a neurodegenerative disease, with an insidious onset and slow (usually years) progression.


person may behave very differently as a result of their illness. For instance, someone who was previously very quiet and unassuming might become loud and aggressive and use offensive language. Some people become withdrawn, while others may become disinhibited or even sexually inappropriate by exhibiting sexual behaviour in public.

Family history

Is positive in 50%.

Dementia with Lewy bodies (DLB)

Takes its name from abnormal collections of protein within nerve cells, known as Lewy bodies.


In addition to symptoms of Alzheimer's disease, people with DLB are likely to experience hallucinations (particularly visual ones) and delusions. The condition tends to have an insidious onset, fluctuates, and parkinsonism is common. DLB is also associated with Parkinson's disease (however it can occur without this). Many features are similar to those seen in delirium (e.g. fluctuations, effect of drugs, psychosis—hallucinations and delusions). DLB often progresses more rapidly than Alzheimer's disease.


Is frequently clinical after excluding the aforementioned reversible causes with neuroimaging and graded by cognitive screens such as the MMSE, and Addenbrooke’s Cognitive Examination-Revised (ACE-R).


This is a screening tool to assess cognitive function. The maximum score is 30. A score of ≤23 is the cut-off point for significant impairment.


The unfamiliar surroundings of the hospital environment are likely to make confusion worse. It can be very disorienting having lights on all the time. These patients are best nursed by the same people in a calm environment, with large wall clocks to help them orientate to time. Be patient. It may be impossible to get a reliable history from the patient so seek other sources of information, including relatives, carers, GP, and previous medical records. Pharmacological treatment for Alzheimer’s disease is with acetylcholine esterase inhibitors such as galantamine and the NMDA receptor antagonist memantine. MDT discussions involving specialist nurses, therapists, psychiatrists, and counsellors with the patient and their families are critical at diagnosis.

Neurology: in the emergency department

Status epilepticus


Prolonged seizure or series of seizures lasting ≥5 min (newly defined as when anticonvulsants are started), or when a second seizure occurs without recovering consciousness from the first during the same time period. This could lead to incomplete recovery often defined after 30 min duration but emergency treatment begins much earlier.


You will see doctors following the ‘ABC Don’t Ever Forget Glucose’ approach:

  • A: airway, recovery position in case airway is compromised from low GCS score and obstructive vomitus/tongue.

  • B: high-flow oxygen.

  • C: venous access, bloods (FBC, U&E, CRP, LFT, Ca2+, Mg2+, antiepileptic drug concentration), venous/arterial blood gases.

  • D: hypoglycaemia is quickly corrected with IV 50% glucose.

  • Check blood glucose and serum electrolytes from a quick venous blood gas test.

Many seizures will self-terminate after a 5 min, but if not, initial treatment is with a benzodiazepine such as IV lorazepam or diazepam; buccal midazolam or PR diazepam in the community. Repeat this dose 10 min later if still fitting, but if not subsiding escalate to IV anticonvulsant loading (over 20 min), usually phenytoin, before escalation to intubation and general anaesthesia (IV propofol, midazolam, or thiopental) in an intensive care setting. EEG may be used to monitor termination of seizure activity. True status epilepticus is a medical emergency with a 20% mortality rate, causing irreversible brain damage in survivors.


5 mL of serum and 50 mL of urine samples should be saved for future analysis, including toxicology, especially if the cause of the convulsive status epilepticus is uncertain. CXR if there is concern about aspiration. Consider CT head and LP if an intracranial lesion or meningitis is suspected.

Clinical tips

Check for head injuries (can be cause or consequence of seizure). If alcohol abuse is suspected, give IV thiamine (Pabrinex®). Be aware of pseudo-seizures (often in psychiatric patients). Advise the patient not to drive if discharged (see Driver and Vehicle Licensing Agency (DVLA) guidance).

Seizure and epilepsy

Patients with ‘fits, faints, and funny turns’ commonly present to neurologists. The diagnosis usually lies in the history of the attack, which is best supplemented by a collateral history from a witness.


Ask about the temporal pattern of attacks, and symptoms between attacks. Are the attacks stereotyped? Talk through a typical attack and identify the timings and what happens before, during, and after.

In attacks with loss of consciousness, identify the first clear memory on regaining consciousness. It is important to elicit the before (aura, triggers, prodromes, warning signs), during (loss of consciousness, head injury, eyewitness account for duration of seizure, foaming at mouth, tongue biting, limb jerking, urinary/faecal incontinence) and after (feeling weak/tired, memory of event, aftermath symptoms) the event.


Is an episode of abnormal synchronous brain electrical activity.


Is the tendency to have recurrent unprovoked seizures.

Generalized seizures

Originate with discharges in both hemispheres, so consciousness is always affected. The classic form we tend to think about is the tonic–clonic seizure, where usually without warning the patient becomes rigid and unresponsive, associated with tongue biting and incontinence. Synchronous jerking of all four limbs typically lasts for a few minutes, reducing in frequency until stopping. Afterwards, the patient is drowsy and confused (‘post-ictal’) for minutes to hours, and once fully recovered will have no recollection of events during the attack and poor recollection of events during the post-ictal state.

Partial (focal) seizures

Originate from a localized area, the clinical manifestations of which depend on the parts of the brain involved. They may be ‘simple’ or ‘complex’, depending on whether awareness is preserved or altered respectively. There may be secondary generalization, where the abnormal discharges spread into a generalized seizure. After a partial seizure in the motor cortex, the affected limb may be weak in the post-ictal state (Todd’s paresis). The most common site of onset for partial seizures is the temporal lobe, causing odd symptoms such as olfactory hallucinations, déjà vu, and motor automatisms.


Seizures may be caused by an idiopathic epilepsy syndromes or be secondary to an underlying brain disorder such as hypoxia, head injury, infection, or metabolic derangement; or a focal lesion such as a tumour, stroke, or vascular malformation.


Since epilepsy is a condition of attacks, examination and investigation in between attacks may be normal. EEG can be helpful and brain imaging can look for an underlying cause, especially in focal seizures.


Is primarily with anticonvulsant drugs, such as lamotrigine or carbamazepine for focal, and sodium valproate for generalized seizures—the choice of which frequently depends on their side effect profiles. Surgery may be an option if there is an underlying resectable structural lesion which is proven to be the epileptic focus.


Not all episodes of collapse and shaking are seizures, and not all seizures cause collapse and shaking. A common mimic is syncope, a transient loss of consciousness due to cerebral hypoperfusion; this is common and results from vasovagal, postural hypotension, cardiac, or carotid sinus disease.

Thunderclap headache

Sudden severe headache which reaches peak severity within 60 sec is termed ‘thunderclap’, which when occurring spontaneously (e.g. non-traumatic) is frequently associated with SAH following rupture of an intracranial berry aneurysm.

Clinical manifestations

Vary: there may be neck stiffness and photophobia due to meningeal irritation; a pupil-involving third nerve palsy may be present due to compression by an underlying posterior communicating artery aneurysm; while focal signs such as hemiparesis can occur due to vasospasm and infarction. Reduced conscious level can occur due to hydrocephalus (non-obstructing CSF accumulation due to impaired resorption).


CT is first performed, which if negative is followed by LP performed 12 hours after headache onset to analyse for xanthochromia, a haemoglobin degradation product.


Confirmed SAH requires angiography to find the culprit aneurysm and secure it by surgical clipping or endovascular coiling.

Stroke and transient ischaemic attack


Any acute neurological deficit with a cerebrovascular cause, strokes and TIAs are rather arbitrarily differentiated by neurological deficits lasting for longer (stroke) or less (TIA) than 24 hours.


Strokes can be caused by ischaemic arterial occlusion (80%) or intracranial haemorrhage (20%); it is important to differentiate on initial diagnosis with imaging because the treatment is obviously distinct.


The Recognition Of Stroke In the Emergency Room (ROSIER) scale is designed to aid diagnosis:

New acute onset (or on awakening from sleep):

• Asymmetric facial weakness


• Asymmetric arm weakness


• Asymmetric leg weakness


• Speech disturbance


• Visual field defect


• Seizure activity


• LOC/syncope


Scores can range from −2 to +5. Stroke is likely if total score is >0 and unlikely if ≤0.


Aim to find the underlying cause of the stroke: carotid Doppler US for carotid artery stenosis, 24-hour ECG for tachyarrhythmias, echocardiograms for cardiac regional wall and valvular abnormalities, in addition to blood tests for DM and lipid disorders. The aim on discharge is optimization of vascular risk factors to prevent further strokes (so-called secondary prevention).

The NIHSS (National Institutes of Health Stroke Scale) is a tool used to quantify the impairment from a stroke (Neurology

  • Bloods (beta-2 microglobulin, FBC, U&E, ESR, blood glucose), ECG (AF is a risk factor), CXR.

  • CT head immediately if any of the following apply:

    • Indications for thrombolysis or anticoagulation.

    • On anticoagulant.

    • A known bleeding tendency.

    • GCS score <13.

    • Unexplained progressive/fluctuating symptoms.

    • Papilloedema, neck stiffness, fever, headache.


When the time of onset is unclear, such as patients who present with deficits on waking, CT perfusion determines whether an ischaemic penumbra exists, where an area of salvageable brain tissue exists around an infarct and hence could make thrombolysis potentially therapeutic. MRI is increasingly available for acute infarcts when ischaemic strokes are difficult to distinguish from mimics such as seizures, migrainous syndromes, intracranial tumours, and demyelinating disease. Know the mechanism of drug action of some of the common thrombolytics prior to shadowing the stroke registrar.


Ischaemic stroke

Typically treated with 300 mg aspirin (exclude haemorrhagic stroke first and supplement with PPI if history of dyspepsia) for 2 weeks followed by 75 mg clopidogrel.

Haemorrhagic stroke

If the patient is anticoagulated, normalize INR using prothrombin complex concentrate and IV vitamin K. Patients are admitted onto a hyperacute stroke unit with specialist stroke physicians, therapists, and dieticians, an arrangement proven to improve survival. Maintain blood glucose level between 4 and 11 mmol/L. Only control BP if there is a hypertensive emergency or for thrombolysis candidates with BP >185/110 mmHg. Swallow screen on admission.


Ischaemic strokes presenting within 4.5 hours of onset may be eligible for thrombolysis treatment, intended to break up the offending arterial blood clot (but with a significant risk of intracranial haemorrhage). Thrombolysis with alteplase (tissue plasminogen activator) if <4.5 hours from onset (current NICE guidance although controversial—direct comparisons of alteplase with no alteplase at 3–4.5 hours after stroke suggest an absolute Neurology in mortality of 2% and no clear benefit).

TIA: ABCD2 system

The ABCD2 scoring system helps identify those at high early risk of stroke as follows.


(Points allocated.)

  • Age (≥60 years = 1).

  • BP (systolic >140 mmHg and/or diastolic ≥90 mmHg = 1).

  • Clinical features (unilateral weakness = 2, speech disturbance without weakness = 1, other = 0).

  • Duration of symptoms in minutes (≥60 = 2, 10–59 = 1, <10 = 0).

  • Diabetes (present = 1).

Risk of stroke in next 2 days based on total score: score of 0–3, risk = 1%; score of 4–5, risk = 4%; score of 6–7, risk = 8%.


Admit high-risk patients: ABCD2 score of ≥4 or those with crescendo TIA (two or more TIAs in a week). Aspirin (300 mg daily) started immediately. Specialist assessment and investigation within 24 hours of onset if high risk, and 7 days if low risk (ABCD2 ≤3). Measures for secondary prevention (e.g. BP and cholesterol control, smoking cessation). If carotid artery imaging (Doppler) shows significant stenosis, carotid endarterectomy should be performed within 2 weeks of the TIA.

Guillain–Barré syndrome

An autoimmune-mediated peripheral neuropathy triggered by GI or lower respiratory infections, classically includes mycoplasma pneumoniae, CMV, and EBV.


Progressive ascending weakness with absent reflexes, and sometimes sensory loss or back pain.


Is based on clinical suspicion and may be supported by block of peripheral nerve conduction on electrophysiological testing and Neurologyprotein on CSF. Autonomic nerves can also be involved and you should be able to thereby explain some of the other wider manifestations of Guillain–Barré syndrome.


May involve IV immunoglobulin or plasma exchange.

CNS infections

Organisms may enter the CNS through the blood, via nerves, or via direct spread from adjacent structures. Infections generally take the form of either meningitis, encephalitis, or a space-occupying lesion. Fever is a common feature to all. Immunosuppression may predispose and a HIV test should be done in all patients with CNS infection.

Bacterial meningitis


Acute neck stiffness, photophobia, headache, and fever. Beware of additional features such as seizures, cranial neuropathies, and systemic features if the patient becomes septic.

Risk groups

Meningitis should be particularly suspected in high-risk groups, such as patients with skull trauma, CSF shunts, and systemic immunosuppression who may present with more uncommon organisms (e.g. TB).


Is made via a combination of clinical features, blood tests, and CSF examination unless contraindicated. CSF in meningitis typically demonstrate raised white blood cells, predominantly neutrophils in bacterial meningitis and lymphocytes in TB, raised proteins, and CSF glucose below 40% of serum levels.


Is with prompt initiation of third-generation IV cephalosporins until the organism is isolated and particular attention paid to complications such as features of raised ICP and seizures. The European Dexamethasone Study1 demonstrated that the use of steroid reduced morbidity and mortality in Streptococcus pneumonia type.

Viral encephalitis


The majority of viral infection of the brain parenchyma results from HSV, EBV, CMV, VZV, and enteroviruses.


Like all infections of the brain, it can involve headache, confusion, seizures, or focal neurology, and can be complicated by combination with meningitis (meningoencephalitis).


Is made clinically, supported by raised serum inflammatory markers and positive viral serology in blood, lymphocytosis, raised protein, and viral serology in CSF; neuroimaging may demonstrate non-specific areas of oedema or haemorrhage.


Patients should be promptly treated with IV aciclovir.


1. de Gans J, van de Beek D, European Dexamethasone in Adulthood Bacterial Meningitis Study Investigators. Dexamethasone in adults with bacterial meningitis. N Engl J Med 2002;347(20):1549–56.Find this resource:

Neurology: in exams

During your neurology placement, ensure that you can perform and elicit the symptoms and signs described in this section.

History station

Cover all the usual areas including family and social history. Ask in detail about function and any practical limitations, e.g. with walking or writing. Ask about driving, which may be limited by law in many neurological diseases. Neurological problems can be very difficult to describe, so be ready to ask discriminating questions that will narrow the differential. For example, if faced with weakness, always ask if there is associated sensory disturbance, and vice versa. If dealing with visual loss, work out if the problem is in one eye or in one visual field—what happens when the patient closes each eye in turn? If a patient uses the word ‘numb’, ask what they mean—insensitive, painful, clumsy, or weak?

Always ask: what is the time course? A sudden onset and slow recovery is typical of vascular events such as stroke. A relapsing–remitting course where symptoms come on over hours or days, reach a peak, and then gradually fade away, with multiple attacks, perhaps with incomplete recovery in between, is typical of inflammatory diseases such as MS. A progressive course is typical of neurodegenerative conditions such as Parkinson’s disease and expanding structural lesions such as tumours. Finally, paroxysmal disorders are characterized by stereotyped attacks, with relatively symptom-free periods in between attacks. Examples of paroxysmal disorders are epilepsy, migraine, and TIAs. Are the symptoms positive or negative? Examples of positive symptoms would be abnormal movement of a limb, or flashing lights in the vision, whereas the converse negative symptoms would be paralysis or loss of vision. Are the symptoms stereotyped—exactly the same with each attack? Are the attacks provoked or unprovoked? Epilepsy tends to cause unprovoked, stereotyped attacks, lasting less than a few minutes, and which may feature positive symptoms and/or altered consciousness. Migraine aura causes positive symptoms which evolve over minutes. TIAs tend to cause negative symptoms which are maximal at onset, and rarely affect consciousness.

When taking a history of loss of consciousness, a collateral history from a witness is essential. Ask the patient exactly what they remember leading up to the attack, and the first thing they remember afterwards. If the patient collapsed, ask if they remember hitting the floor. Ask the witness what they observed before, during, and after the attack, including any abnormal movements or colour change. Finally, ensure that your history has covered the major elements of the nervous system: limbs, eyes, face, swallowing, speech, bladder/bowel, and cognition.

Things to do

Lumbar puncture

You need to be competent to perform this on clinical models. See Table 22.4 for CSF analysis. Be prepared to answer:

  • What structures does the needle pass through?

    • Skin, subcutaneous fat, supraspinous and interspinous ligaments, ligamentum flavum, epidural space, dura, subarachnoid space, CSF.

  • Where does the spinal cord end?

    • Between L1 and L2; below this level the nerve roots float in the subarachnoid space as the cauda equine and safe space for LP.

  • What is the normal CSF pressure?

    • Vary between 8–16 cm water but >20 cm water is abnormal.

  • What is the CSF volume and how quickly is it made?

    • Volume is ~120 mL, and 500 mL are made (and reabsorbed)/day.

Table 22.4 CSF analysis





Pressure (cmH2O)










Protein (g/L)





Glucose (4.4 mmol/L)





Gram stain


Positive >60%



Glucose CSF:serum





WCC (/mm3)



(90% PMN)


(monocytes with some PMN)


Neurology examination

Holding the arm flexed and leg extended is common in hemiparesis. Look for movement disorders, which broadly speaking feature either too little movement (akinetic-rigid syndromes including Parkinson’s disease), too much movement (hyperkinetic disorders including chorea), or abnormal postures (dystonia). Also look around the patient, for functional aids or signs of treatment before inspecting the gait. Ask the patient to get out of the chair or bed without using their arms—a good test for proximal weakness. Test for Romberg’s sign—ask the patient to stand with their feet together and arms by their side, then to close their eyes. The sign is positive if the patient is steady with eyes open but unsteady with eyes closed, and implies sensory ataxia (loss of joint position sense). Then assess gait, walking normally, and then heel–toe to bring out the unsteadiness of cerebellar ataxia.