Learn — Neurological

15 notes · 62 questions on the topic

Glasgow Coma Scale (GCS)

The Glasgow Coma Scale is a standardised measure of impaired consciousness that scores the best eye opening out of 4, the best verbal response out of 5 and the best motor response out of 6, giving a total from 3 to 15. It matters because a single number, recorded the same way by every observer and repeated over time, is what shows that a brain is deteriorating, and it drives three decisions: whether to intubate, whether to scan, and when to call the neurosurgeon.

Eye opening out of 4: 4 spontaneous, 3 to sound or speech, 2 to pressure or pain, 1 none; record NT (not testable) when the eyes are swollen shut rather than scoring 1.
Verbal response out of 5: 5 orientated in person, place and time, 4 confused conversation, 3 inappropriate words, 2 incomprehensible sounds, 1 none; record T when the patient is intubated, because a tube is not a score of 1.
Motor response out of 6: 6 obeys commands, 5 localises to a central painful stimulus, 4 normal flexion or withdrawal from pain, 3 abnormal flexion or decorticate posturing (arms flexed across the chest with legs extended, a lesion above the red nucleus), 2 extension or decerebrate posturing (arms extended and internally rotated, a brainstem lesion), 1 none.
Score the best response on the best side: if the right arm localises and the left extends, the motor score is 5. Use a central stimulus such as trapezius pinch or supraorbital pressure to test localisation, and a peripheral stimulus such as nail bed pressure to test flexion and withdrawal.
Severity bands: 13 to 15 is mild head injury, 9 to 12 moderate and 3 to 8 severe. A GCS of 8 or less means the patient cannot protect the airway, so the rule is GCS 8, intubate; a fall of 2 or more points from any starting level is the trigger for immediate reassessment, an urgent CT and a call to the neurosurgeon.
Always record the three components separately, because a total of 8 made of E2 V2 M4 is a very different patient from E1 V1 M6; the motor score carries most of the prognostic weight, and a total of 3 with fixed dilated pupils carries the worst prognosis.
Confounders must be excluded before a low score is attributed to the brain: sedation, neuromuscular blockade, alcohol and drugs, hypoglycaemia, hypoxia, hypotension, hypothermia, post-ictal state and a language barrier. Check the capillary glucose in every unconscious patient before anything else.
The paediatric modification changes only the verbal scale for the pre-verbal child — 5 coos, babbles or is appropriately interactive, 4 irritable cry that is consolable, 3 cries to pain, 2 moans to pain, 1 none — and substitutes spontaneous purposeful movement for obeying commands in the motor scale.
Observation schedule after head injury: half-hourly GCS with pupils, limb power, pulse, blood pressure, respiratory rate, temperature and oxygen saturation until the GCS reaches 15, then half-hourly for 2 hours, hourly for 4 hours and two-hourly thereafter, restarting at half-hourly if the patient deteriorates.

Head injury — EDH and SDH

An extradural (epidural) haematoma is a collection of blood between the skull and the dura, almost always from a torn middle meningeal artery beneath a temporal or parietal fracture, while a subdural haematoma lies between the dura and the arachnoid and comes from torn bridging veins. Both matter because the primary impact injury is already fixed by the time the patient arrives, but the secondary injury from an expanding clot, hypoxia, hypotension and raised intracranial pressure is preventable — and it is the nurse's serial observations that catch it.

Extradural haematoma: typically a young patient, temporo-parietal, arterial, biconvex or lens-shaped on CT, limited by the sutures so it does not cross them but able to cross the midline, with an overlying skull fracture in the great majority. The classic course is a brief loss of consciousness, a lucid interval of minutes to hours, then rapid deterioration with an ipsilateral fixed dilated pupil and contralateral hemiparesis; evacuated early, the outcome is excellent.
Subdural haematoma: crescentic and concave on CT, crossing suture lines but limited by the falx at the midline; acute (under 3 days, hyperdense), subacute (3 days to 3 weeks, isodense and easy to miss) and chronic (over 3 weeks, hypodense). Chronic subdural haematoma is the disease of the elderly, the alcoholic and the anticoagulated after trivial or forgotten trauma, presenting with headache, confusion, a fluctuating conscious level or a stroke-like picture, and it is drained through burr holes; acute subdural carries a far worse prognosis than extradural because the brain underneath is also injured.
The Monro-Kellie doctrine explains the physiology: the skull is a rigid box containing brain, blood and cerebrospinal fluid, and a new mass is compensated by displacing cerebrospinal fluid and venous blood until compensation is exhausted, after which the pressure rises steeply for a small increase in volume. Normal adult intracranial pressure is 5 to 15 mmHg and treatment is started above 22 mmHg.
Cerebral perfusion pressure is the mean arterial pressure minus the intracranial pressure and is kept at 60 to 70 mmHg; the systolic pressure is kept at 110 mmHg or above in adults aged 15 to 49 and over 70, and at 100 mmHg or above between 50 and 69, because a single episode of hypotension or of hypoxia with a saturation under 90% roughly doubles mortality after a severe head injury.
Raised intracranial pressure produces headache, vomiting, papilloedema and a falling conscious level; the Cushing response of rising blood pressure with a widening pulse pressure, bradycardia and irregular or Cheyne-Stokes breathing is a late, pre-terminal sign of brainstem compression, not a reassuring set of observations.
Managing a rising intracranial pressure: nurse head up 30 degrees with the neck straight and no tight collar or tapes obstructing the jugular veins, keep oxygenation normal and the arterial carbon dioxide at 35 to 40 mmHg, sedate and give analgesia, treat fever and seizures, minimise suctioning and cluster the care, and give mannitol 0.25 to 1 g/kg intravenously over about 20 minutes or hypertonic saline. Brief hyperventilation to a carbon dioxide of 30 to 35 mmHg is a rescue measure only, because vasoconstriction reduces cerebral blood flow, and corticosteroids are contraindicated in traumatic brain injury because they increase mortality.
Basal skull fracture is recognised by raccoon or panda eyes, Battle's sign over the mastoid, cerebrospinal fluid rhinorrhoea or otorrhoea (the halo or double-ring sign on a gauze, fluid positive for glucose, or beta-2 transferrin), haemotympanum and cranial nerve palsies. No nasogastric tube through the nose, no nose blowing, no packing the ear or nose, and no attempt to stop the leak — let it drain and watch for meningitis.
Mannitol is an osmotic diuretic, so it is given only with a secured airway and adequate circulating volume; watch the urine output, serum sodium and osmolality, and withhold it if the osmolality is above about 320 mOsm/kg or the patient is hypotensive, because dehydrating a hypotensive patient lowers the cerebral perfusion pressure further.
Nursing observation after head injury: half-hourly GCS with pupil size and reaction, limb power, pulse, blood pressure, respiratory rate, temperature and saturation until the GCS is 15, then half-hourly for 2 hours, hourly for 4 hours and two-hourly after that; a fall of 2 GCS points, a new pupil asymmetry, a seizure, focal weakness, severe or increasing headache or persistent vomiting all mean urgent reassessment and CT.

Parkinson disease

Parkinson disease is a progressive neurodegenerative disorder caused by the loss of dopaminergic neurons in the pars compacta of the substantia nigra, with alpha-synuclein aggregates called Lewy bodies in the surviving cells; motor signs appear only after 60 to 80 per cent of those neurons are gone. It matters because the diagnosis is made at the bedside from the pattern of tremor, rigidity and slowness rather than from a scan, and because the timing of the drugs, not their choice, is what keeps the patient walking and out of hospital.

The cardinal features are remembered as TRAP: a resting pill-rolling tremor at 4 to 6 Hz that lessens on voluntary movement and disappears in sleep, cogwheel rigidity, bradykinesia, and postural instability that comes late. Bradykinesia must be present for the diagnosis, and the signs begin asymmetrically.
Supporting features are a mask-like expressionless face, reduced blinking, soft monotonous hypophonic speech, micrographia, a stooped posture with reduced arm swing, a shuffling festinating gait with freezing at doorways, drooling, seborrhoea and constipation.
Non-motor features often precede the tremor by years — loss of smell, constipation, depression and rapid-eye-movement sleep behaviour disorder in which the patient acts out dreams; later come orthostatic hypotension, urinary urgency, and dementia in advanced disease.
Levodopa combined with a peripheral decarboxylase inhibitor such as carbidopa or benserazide is the most effective drug; the inhibitor prevents peripheral conversion to dopamine and so prevents nausea, and after about five years most patients develop wearing-off, on-off fluctuations and dyskinesias.
Levodopa is taken 30 to 60 minutes before food, because dietary protein competes with it for the same large neutral amino acid transporter across the gut and the blood-brain barrier; it must not be taken with iron, and the doses are time-critical.
The other classes are dopamine agonists such as pramipexole and ropinirole, which cause impulse control disorders and sleep attacks, monoamine oxidase B inhibitors such as selegiline and rasagiline, catechol-O-methyltransferase inhibitors such as entacapone that extend each levodopa dose, amantadine for dyskinesia, and anticholinergics such as trihexyphenidyl for tremor in the young, which are avoided in the elderly because they cause confusion, retention and glaucoma.
Drug-induced parkinsonism is the great mimic and is reversible: metoclopramide, prochlorperazine, haloperidol, risperidone, cinnarizine and flunarizine are the usual culprits, it is typically symmetrical, and the antiemetic of choice in a Parkinson patient is domperidone, with quetiapine or clozapine if an antipsychotic is unavoidable.
Essential tremor is the commonest confusion: it is an action or postural tremor, bilateral, often involves the head and voice, improves with alcohol, has a family history and responds to propranolol, whereas the Parkinson tremor is present at rest, asymmetrical and disappears with action.
Deep brain stimulation of the subthalamic nucleus is offered in advanced disease with disabling motor fluctuations that still respond to levodopa, alongside lifelong physiotherapy with cueing, speech therapy for hypophonia and dysphagia, and occupational therapy for falls and activities of daily living.

Stroke — ischaemic vs haemorrhagic

A stroke is a sudden focal neurological deficit of vascular origin lasting more than 24 hours or accompanied by infarction or haemorrhage on imaging, while a transient ischaemic attack is the same picture that resolves without tissue infarction. The single question that decides everything is whether it is ischaemic or haemorrhagic, because the treatment of one is the poison of the other, and only a plain computed tomography scan of the head can answer it.

About 80 to 85 per cent of strokes are ischaemic — large-artery atherosclerosis, cardioembolism most often from atrial fibrillation, and small-vessel lacunar disease — and 15 to 20 per cent are haemorrhagic, split between intracerebral haemorrhage, typically hypertensive and in the basal ganglia, and subarachnoid haemorrhage from a ruptured berry aneurysm.
Recognition uses BE-FAST — sudden Balance loss, Eyes or visual loss, Face droop, Arm weakness, Speech disturbance, Time to call — and severity is scored with the National Institutes of Health Stroke Scale, which also guides treatment decisions.
A non-contrast computed tomography scan is done first and solely to exclude haemorrhage; it may look normal in the first hours of an infarct, so a normal scan in a patient with a deficit supports, and does not exclude, ischaemia. Diffusion-weighted magnetic resonance imaging shows infarction within minutes.
Intravenous thrombolysis with alteplase 0.9 mg/kg to a maximum of 90 mg, given as 10 per cent by bolus over 1 minute and the rest over 60 minutes, is offered within 4.5 hours of the time the patient was last known well; tenecteplase 0.25 mg/kg as a single bolus is an accepted alternative. Mechanical thrombectomy treats large-vessel occlusion up to 24 hours from onset in patients selected by perfusion imaging.
Blood pressure rules differ by pathway: before thrombolysis it must be brought below 185/110 mmHg and kept below 180/105 mmHg for 24 hours afterwards; in an ischaemic stroke not being thrombolysed, hypertension is permitted and treated only above about 220/120 mmHg; in intracerebral haemorrhage the systolic pressure is lowered carefully to around 140 mmHg.
Absolute contraindications to thrombolysis include any previous intracranial haemorrhage, ischaemic stroke or serious head injury within 3 months, active internal bleeding, a platelet count under 100000/mm3, an international normalised ratio above 1.7, and a blood pressure that will not come below 185/110 mmHg.
Check the capillary blood glucose in every suspected stroke, because hypoglycaemia is the commonest stroke mimic along with seizure with Todd paresis, migraine with aura and conversion disorder; correct a glucose under 60 mg/dL immediately and then keep it in the 140 to 180 mg/dL range.
If the patient is not thrombolysed, give aspirin 300 mg within 24 to 48 hours; after thrombolysis, no antiplatelet, anticoagulant, intramuscular injection, arterial puncture, nasogastric tube or urinary catheter for 24 hours, and a repeat scan before antiplatelets are started.
The time targets are what the exam wants: door to computed tomography within 25 minutes and door to needle within 60 minutes, with the mantra that time is brain and about 1.9 million neurons are lost every minute an occlusion continues.
Secondary prevention is antiplatelet or anticoagulation for atrial fibrillation, a high-intensity statin, blood pressure and diabetes control, smoking cessation, and carotid endarterectomy for a symptomatic internal carotid stenosis of 70 to 99 per cent.

Myasthenia gravis

Myasthenia gravis is an autoimmune disease in which antibodies against the postsynaptic nicotinic acetylcholine receptor at the neuromuscular junction, or against muscle-specific kinase, reduce the number of working receptors and produce weakness that worsens with use and recovers with rest. It matters because the fatigability is diagnostic at the bedside, and because the same disease that begins as a drooping eyelid can end in respiratory failure within hours when the bulbar and intercostal muscles are drawn in.

The hallmark is fatigable weakness: worse at the end of the day and after repeated effort, better after rest, with normal sensation, preserved deep tendon reflexes and spared pupils. Spared pupils separate it from botulism, which gives fixed dilated pupils with descending paralysis.
It has a bimodal onset, in women in their twenties and thirties and in men over sixty. About half present with purely ocular symptoms of asymmetric ptosis and diplopia, and roughly 80 per cent of those generalise within 2 years to bulbar, neck and proximal limb weakness.
Bulbar involvement shows as nasal regurgitation, a nasal voice that fades as the patient talks, difficulty chewing halfway through a meal and a weak neck that makes the head droop; these are the features that predict aspiration and crisis.
Bedside tests are the ice pack test, in which ice held over the closed lid for about 2 minutes improves the ptosis because cooling inhibits acetylcholinesterase, and the fatigue test of sustained upgaze; the edrophonium or Tensilon test is now of historical interest.
Confirmation is by acetylcholine receptor antibodies, positive in about 85 per cent of generalised and half of ocular cases, with anti-muscle-specific kinase antibodies in seronegative patients, a decremental response of more than 10 per cent on repetitive nerve stimulation, and single-fibre electromyography as the most sensitive test. A computed tomography scan of the chest is mandatory because 10 to 15 per cent have a thymoma and most of the rest have thymic hyperplasia.
Treatment is symptomatic with pyridostigmine, typically 30 to 60 mg every 4 to 6 hours, and immunological with corticosteroids, azathioprine or mycophenolate; thymectomy is done for any thymoma and for generalised antibody-positive disease in younger patients. Intravenous immunoglobulin 2 g/kg over 2 to 5 days or plasma exchange is used for crisis and before surgery.
Myasthenic crisis is respiratory failure from the disease and is monitored by forced vital capacity, single-breath count and negative inspiratory force, not by pulse oximetry, because saturation falls only when the patient is nearly arrested; a forced vital capacity falling below about 15 to 20 mL/kg or a single-breath count under 20 calls for intensive care and elective intubation.
Cholinergic crisis is the mirror image, caused by too much anticholinesterase, and shows the muscarinic excess of salivation, lacrimation, urination, diarrhoea, abdominal cramping, bradycardia, small pupils and muscle fasciculation; the safe management of either is to withhold pyridostigmine, support ventilation and treat with immunotherapy.
Drugs that worsen myasthenia and must be checked before they are given include aminoglycosides, fluoroquinolones, macrolides, beta blockers, calcium channel blockers, magnesium sulphate, phenytoin, quinine, chloroquine, penicillamine and neuromuscular blocking agents.

Epilepsy — types and management

Epilepsy is a disorder of the brain defined by at least two unprovoked seizures more than 24 hours apart, or by one unprovoked seizure with a recurrence risk of at least 60 per cent over the next 10 years, or by the diagnosis of an epilepsy syndrome. It matters because the seizure type dictates the drug — the wrong choice makes some seizures worse — and because a convulsion that has lasted 5 minutes has become status epilepticus and is a medical emergency that the nurse starts treating.

The 2017 International League Against Epilepsy classification starts from the onset: focal, generalised or unknown. Focal seizures are then divided by awareness into focal aware and focal impaired awareness, by motor or non-motor onset, and by whether they evolve to a bilateral tonic-clonic seizure; generalised seizures are tonic-clonic, absence, myoclonic, atonic, tonic or clonic.
Childhood absence epilepsy gives brief blank spells with no aura and no post-ictal confusion, is provoked by 3 minutes of hyperventilation, shows a 3 Hz generalised spike-and-wave discharge, and is treated with ethosuximide or valproate. Juvenile myoclonic epilepsy gives early-morning jerks provoked by sleep deprivation.
Carbamazepine, oxcarbazepine, phenytoin and gabapentin can make absence and myoclonic seizures worse, which is the classic discriminator in a question about a child whose blank spells increased after treatment.
First-line drugs: levetiracetam, lamotrigine or carbamazepine for focal seizures; valproate, levetiracetam or lamotrigine for generalised seizures; ethosuximide for absence. Valproate is avoided in girls and women of childbearing potential because of neural tube defects and impaired neurodevelopment, and it is used only under a pregnancy prevention programme.
Know the drug hazards: phenytoin follows zero-order kinetics so a small dose rise causes toxicity with nystagmus, ataxia and slurred speech, and it causes gum hypertrophy and hirsutism; intravenous phenytoin is diluted in normal saline and never in dextrose, is given no faster than 50 mg/min with cardiac and blood pressure monitoring, and can cause purple glove syndrome. Carbamazepine causes hyponatraemia and, in patients carrying HLA-B*1502, severe skin reactions.
Status epilepticus is operationally defined as a convulsion lasting 5 minutes or more, or repeated seizures without recovery of consciousness in between; 30 minutes is the point at which neuronal injury begins, which is why treatment starts at 5.
The status ladder is fixed and worth memorising: airway, oxygen, lateral position and a capillary glucose in the first 5 minutes; then a benzodiazepine — intravenous lorazepam 0.1 mg/kg to a maximum of 4 mg per dose, repeated once, or intramuscular midazolam 10 mg when there is no line; then a second-line intravenous drug at 20 to 40 minutes, either levetiracetam 60 mg/kg, fosphenytoin or phenytoin 20 mg/kg phenytoin-equivalent, or valproate 40 mg/kg; then anaesthesia with midazolam, propofol or thiopentone under intubation and electroencephalogram control.
Always look for the provoked causes before labelling epilepsy: hypoglycaemia, hyponatraemia, hypocalcaemia, alcohol withdrawal, drug overdose, head injury, meningitis, neurocysticercosis, which is a leading cause of adult-onset seizures in India, and eclampsia in pregnancy, where the drug is magnesium sulphate and not a conventional anti-seizure medicine.
Living with epilepsy is part of the answer: take the drug at the same time daily because non-adherence is the commonest cause of breakthrough seizures, keep a seizure diary, avoid swimming alone, heights, unguarded machinery and driving until the legal seizure-free period is met, take folic acid before conception, and know that enzyme-inducing drugs reduce the effectiveness of oral contraceptives.

Guillain-Barre syndrome

Guillain-Barre syndrome is an acute immune-mediated polyradiculoneuropathy in which antibodies raised against a preceding infection cross-react with peripheral nerve myelin or axons, producing rapidly progressive symmetrical flaccid weakness with areflexia. It is now the commonest cause of acute flaccid paralysis worldwide since polio control, and it matters because the patient stays fully conscious while the diaphragm quietly fails, so the nurse who measures the vital capacity is the one who prevents the arrest.

Two to four weeks before the weakness there is usually an infection — Campylobacter jejuni is the commonest and is linked to the axonal forms and a worse outcome, followed by cytomegalovirus, Epstein-Barr virus, Mycoplasma, hepatitis E and Zika virus.
The weakness is symmetrical and ascends from the legs upwards, with early loss of deep tendon reflexes, tingling and back or limb pain but only minor objective sensory loss; the deficit reaches its worst within 4 weeks by definition, most often within 2, and then plateaus before slow recovery.
Cranial nerve involvement gives bilateral facial weakness and bulbar palsy with a poor cough and difficulty swallowing; the Miller Fisher variant is the triad of ophthalmoplegia, ataxia and areflexia and carries anti-GQ1b antibodies.
Autonomic dysfunction occurs in most severe cases and is a cause of sudden death: swings between hypertension and hypotension, tachyarrhythmias and bradyarrhythmias especially during suction, ileus, urinary retention and abnormal sweating, so continuous cardiac monitoring is part of the care.
Cerebrospinal fluid shows albuminocytological dissociation — a raised protein with a cell count below 50/mm3 — but this typically appears only after the first week, so a normal early tap does not exclude the diagnosis. Nerve conduction studies show conduction block, prolonged distal latencies and abnormal F waves.
Respiratory failure is anticipated, not reacted to: measure the forced vital capacity and the single-breath count every 2 to 4 hours and apply the 20/30/40 rule — a forced vital capacity below 20 mL/kg, a maximum inspiratory pressure less negative than minus 30 cmH2O, or a maximum expiratory pressure below 40 cmH2O calls for elective intubation. Oxygen saturation stays normal until the patient is nearly exhausted.
Treatment is intravenous immunoglobulin 0.4 g/kg a day for 5 days or plasma exchange; the two are equally effective, are not combined, and work best when started within 2 weeks of onset. Corticosteroids are ineffective in Guillain-Barre syndrome and are not used, which is a frequently examined point.
Supportive nursing is most of the treatment: thromboprophylaxis, two-hourly turning and pressure area care, passive range-of-motion exercises and splinting to prevent contractures and foot drop, bowel and bladder care, eye care and taping in facial palsy, nutrition, and neuropathic pain relief with gabapentin or carbamazepine rather than escalating opioids.
The patient is awake, aware and often terrified inside a paralysed body, so establish a communication system such as a letter board or eye signals early, explain every procedure, and involve the family; suxamethonium is avoided during intubation because of the risk of fatal hyperkalaemia.

Multiple sclerosis

Multiple sclerosis is a chronic immune-mediated inflammatory disease in which the myelin of the central nervous system is attacked, producing plaques of demyelination and, later, axonal loss and permanent disability. The diagnosis rests on lesions disseminated in space and in time, so the exam question is almost always a young woman with two neurological events in different parts of the central nervous system separated by an interval.

It affects women two to three times as often as men, usually begins between 20 and 40 years, and is commoner further from the equator; low vitamin D, Epstein-Barr virus infection and smoking are the recognised risk factors.
About 85 per cent begin as relapsing-remitting disease, which over years may become secondary progressive; 10 to 15 per cent are primary progressive from the start, and a first single episode is called a clinically isolated syndrome.
Characteristic presentations are optic neuritis with painful monocular visual loss, pain on eye movement, a relative afferent pupillary defect and red desaturation; internuclear ophthalmoplegia from a medial longitudinal fasciculus lesion; the Lhermitte sign of an electric shock down the spine on neck flexion; and the Uhthoff phenomenon in which heat, a hot bath or a fever transiently worsens the symptoms.
The everyday burden is fatigue, spasticity, ataxia and tremor, bladder urgency or retention, constipation, sexual dysfunction, neuropathic pain, and trigeminal neuralgia occurring at an unusually young age.
Diagnosis uses the 2017 revision of the McDonald criteria; magnetic resonance imaging shows ovoid periventricular plaques perpendicular to the ventricles known as Dawson fingers, together with juxtacortical, infratentorial and spinal cord lesions, and cerebrospinal fluid oligoclonal bands are found in over 85 per cent and can stand in for dissemination in time.
An acute relapse is treated with high-dose methylprednisolone, typically 1 g intravenously daily for 3 to 5 days, which shortens the attack but does not change long-term disability; plasma exchange is used for a severe steroid-refractory relapse.
Disease-modifying therapy reduces the relapse rate and includes interferon beta, glatiramer acetate, teriflunomide, dimethyl fumarate, fingolimod, natalizumab, cladribine and ocrelizumab; natalizumab carries a risk of progressive multifocal leukoencephalopathy in patients positive for JC virus antibodies, so serology and vigilance for new deficits are mandatory.
A pseudo-relapse is old deficits re-emerging because of fever, a urinary tract infection or heat, and it is treated by treating the infection and cooling the patient, not by a course of steroids — so a urine culture comes before the methylprednisolone in a patient who is febrile.
Nursing care is about function and prevention: energy conservation and planned rest for fatigue, avoiding hot baths and treating fever promptly, baclofen or tizanidine with stretching for spasticity, bladder training or clean intermittent self-catheterisation with prompt treatment of infection, falls and pressure area prevention, bowel regulation, vitamin D, and counselling on pregnancy, in which relapses fall during gestation and rise in the first months after delivery.

Alzheimer dementia

Alzheimer disease is the commonest cause of dementia, accounting for roughly 60 to 70 per cent of cases, and is a progressive neurodegeneration marked by extracellular beta-amyloid plaques and intracellular neurofibrillary tangles of hyperphosphorylated tau, beginning in the entorhinal cortex and hippocampus. Dementia itself is an acquired, progressive decline in two or more cognitive domains that interferes with daily function while consciousness remains clear, and that last phrase is what separates it from delirium at the bedside.

The course is stereotyped: early loss of recent episodic memory with repetitive questioning and misplaced objects, then word-finding difficulty and getting lost in familiar places, then apraxia, agnosia, wandering and sundowning, and finally incontinence, immobility and dysphagia, with aspiration pneumonia the usual terminal event.
Age is the strongest risk factor, followed by family history, the APOE epsilon-4 allele, Down syndrome because the amyloid precursor protein gene sits on chromosome 21, previous head injury, low education and untreated vascular risk factors; mutations in the amyloid precursor protein, presenilin-1 and presenilin-2 genes cause the rare early-onset familial disease.
Distinguish delirium from dementia in every confused older patient: delirium comes on over hours to days, fluctuates through the day, impairs attention and the level of consciousness, and is reversible, while dementia comes on over months to years, is stable within a day and leaves consciousness clear. A patient with known dementia who deteriorates suddenly has a delirium on top of it.
Screen with the Mini-Mental State Examination, where a score below 24 out of 30 suggests impairment, or the Montreal Cognitive Assessment, where below 26 out of 30 is abnormal and which is more sensitive for mild cognitive impairment; both are adjusted for education, and the clock-drawing test is a quick bedside supplement.
Always exclude the reversible causes before accepting the diagnosis: vitamin B12 deficiency, hypothyroidism, depression presenting as pseudodementia, neurosyphilis, human immunodeficiency virus infection, chronic subdural haematoma, and normal pressure hydrocephalus with its triad of gait apraxia, urinary incontinence and dementia. Anticholinergic drugs, benzodiazepines and sedating antihistamines are a common and correctable contributor.
Cholinesterase inhibitors — donepezil starting at 5 mg at night and increased to 10 mg, rivastigmine or galantamine — are used for mild to moderate disease and give a modest symptomatic benefit; check the pulse before each dose because they cause bradycardia and syncope, and warn about nausea, diarrhoea, vivid dreams and weight loss.
Memantine, an N-methyl-D-aspartate receptor antagonist, is added for moderate to severe disease; the anti-amyloid monoclonal antibodies lecanemab and donanemab slow decline modestly in early disease, carry a risk of amyloid-related imaging abnormalities with brain oedema and microhaemorrhage, and are not part of routine Indian practice.
Behavioural and psychological symptoms are managed first without drugs — a fixed daily routine, familiar faces, orientation cues, good lighting in the evening to reduce sundowning, activity, and a hunt for pain, constipation, retention, hunger or infection as the trigger. Antipsychotics increase stroke and death in older people with dementia and are used only for severe risk, at the lowest dose and for the shortest time.
Nursing and family care carry the plan: assess safety around cooking, gas, driving, wandering and medicines, label rooms, keep the environment unchanged, give one-step instructions with adequate time, monitor weight and hydration because these patients forget to eat and drink, and address caregiver burnout with respite and support, along with advance care planning while the patient can still take part.

Meningitis

Meningitis is inflammation of the leptomeninges and the cerebrospinal fluid in the subarachnoid space, caused by bacteria, viruses, mycobacteria or fungi. Acute bacterial meningitis is a true emergency in which the first dose of antibiotic should be given within an hour of the patient arriving, because every hour of delay increases death and deafness, while viral meningitis is usually self-limiting — so the whole art is to treat the dangerous one first and stop later.

The organisms follow the age: Group B Streptococcus, Escherichia coli and Listeria in neonates; Streptococcus pneumoniae, Neisseria meningitidis and Haemophilus influenzae type b in children, with the Hib share now much reduced because the vaccine is in the Universal Immunisation Programme; pneumococcus and meningococcus in adults; and Listeria added over 50 years or in the immunocompromised, which is why ampicillin is added to their regimen.
The classic triad of fever, headache and neck stiffness is complete in fewer than half of adults, so a fever with any altered mental state should raise the suspicion; Kernig and Brudzinski signs support it, and a non-blanching petechial or purpuric rash means meningococcal septicaemia.
Infants show none of the classic signs: poor feeding, a high-pitched cry, irritability alternating with lethargy, a bulging anterior fontanelle, seizures and temperature instability with hypothermia rather than fever.
Cerebrospinal fluid tells the four diseases apart. Bacterial fluid is turbid with hundreds to thousands of neutrophils, protein above 100 mg/dL, glucose below 40 mg/dL or a cerebrospinal fluid to blood glucose ratio under 0.4, and a raised opening pressure; viral fluid is clear with lymphocytes, mildly raised protein and normal glucose; tuberculous fluid forms a cobweb coagulum with lymphocytes, very high protein and low glucose; cryptococcal fluid shows lymphocytes with a positive India ink or antigen test.
Computed tomography before the lumbar puncture is required when there is a focal neurological deficit, a new seizure, papilloedema, immunosuppression or a Glasgow coma score of 12 or less, because of the risk of coning; imaging must never delay treatment, so take blood cultures and give the antibiotic first and do the tap afterwards.
Empirical treatment in an adult is intravenous ceftriaxone 2 g twelve-hourly with vancomycin added for resistant pneumococcus, plus ampicillin when Listeria is a possibility; dexamethasone 0.15 mg/kg six-hourly for 4 days is given with or just before the first antibiotic dose, because it reduces death and deafness in pneumococcal meningitis and is useless if given late.
Close contacts of a meningococcal case need chemoprophylaxis: rifampicin 600 mg twelve-hourly for 2 days in adults and 10 mg/kg in children, or a single dose of ciprofloxacin 500 mg, or ceftriaxone 250 mg intramuscularly, which is the choice in pregnancy. The patient is nursed with droplet precautions for the first 24 hours of effective treatment, and the case is notified.
Anticipate the complications: raised intracranial pressure, seizures, the syndrome of inappropriate antidiuretic hormone secretion with hyponatraemia, subdural effusion and hydrocephalus in children, cerebral abscess, and sensorineural hearing loss, so every child gets a hearing assessment after recovery. Meningococcal sepsis can progress to disseminated intravascular coagulation and adrenal haemorrhage in the Waterhouse-Friderichsen syndrome.
Ward care is specific: nurse in a quiet, dimly lit room with the head end raised about 30 degrees, do neurological observations and pupil checks at least hourly at first, keep seizure precautions ready, chart fluids strictly because of the risk of both dehydration and inappropriate antidiuretic hormone, control fever and pain, and give tuberculosis meningitis patients steroids alongside the antitubercular regimen.

Brain oedema — types

Cerebral oedema is an abnormal accumulation of fluid within the brain, either inside the cells or in the extracellular space, which increases brain volume. It matters because the skull is a rigid box: by the Monro-Kellie doctrine the added volume is first compensated by displacing cerebrospinal fluid and venous blood, and once that reserve is used up the intracranial pressure climbs steeply, perfusion falls and the brain herniates.

Vasogenic oedema follows breakdown of the blood-brain barrier, so plasma leaks into the extracellular space of white matter; it is the oedema of tumours, abscesses, meningitis and contusions, and it is the one type that responds to corticosteroids such as dexamethasone.
Cytotoxic oedema is intracellular swelling from failure of the sodium-potassium pump in ischaemia, hypoxia, cardiac arrest or acute hyponatraemia; it involves both grey and white matter, the barrier is intact, and corticosteroids do not help and may harm.
Interstitial or transependymal oedema is cerebrospinal fluid forced across the ependyma in obstructive hydrocephalus, and its treatment is diversion of the fluid by an external ventricular drain or a shunt rather than any drug.
Normal intracranial pressure in an adult is about 5 to 15 mmHg, and treatment is directed at a sustained pressure above 20 to 22 mmHg. Cerebral perfusion pressure is the mean arterial pressure minus the intracranial pressure, and in traumatic brain injury it is kept at about 60 to 70 mmHg, which is why lowering the blood pressure aggressively can starve the brain.
The Cushing response — rising blood pressure with a widening pulse pressure, bradycardia and irregular breathing — is a late sign of impending herniation, not an early warning; earlier signs are a falling Glasgow coma score, a new headache with vomiting, and a sluggish then dilating pupil on the side of the lesion.
First-tier measures are simple and nursing-led: head end raised to 30 degrees with the neck midline and no tight endotracheal tube ties or cervical collar obstructing venous drainage, adequate analgesia and sedation, normothermia, treatment of seizures, avoidance of hypotonic fluids so that normal saline is used and dextrose solutions are not, and keeping arterial carbon dioxide in the normal 35 to 40 mmHg range.
Osmotherapy is either mannitol 20 per cent at 0.25 to 1 g/kg infused over 15 to 20 minutes through a filter, with serum osmolality, sodium, urine output and volume status monitored because it causes an osmotic diuresis and can precipitate hypovolaemia and renal injury, or hypertonic saline 3 per cent, which is preferred when the patient is hypovolaemic or hyponatraemic.
Hyperventilation to an arterial carbon dioxide of 30 to 35 mmHg works within minutes by cerebral vasoconstriction but is only a rescue bridge to definitive treatment, because sustained hypocapnia causes ischaemia; the later tiers are barbiturate coma, therapeutic hypothermia and decompressive craniectomy.
Routine nursing prevents pressure spikes: avoid clustering painful procedures, pre-oxygenate and limit each suction pass to 10 to 15 seconds, prevent straining and the Valsalva manoeuvre with stool softeners and antiemetics, avoid extreme hip flexion, keep the room quiet, and do hourly neurological observations with pupil size and reaction.

Tonic-clonic seizure nursing care

A generalised tonic-clonic seizure is an abrupt loss of consciousness followed by a tonic phase of sustained muscle contraction and then a clonic phase of rhythmic jerking, ending in a post-ictal period of drowsiness and confusion. The nursing care is entirely protective rather than restrictive: nothing stops the seizure once it has begun, so the nurse's job is to keep the airway safe, prevent injury, time the event accurately and know the point at which it becomes status epilepticus.

The sequence to recognise and chart is a sudden cry as air is forced through closed cords, loss of consciousness with a fall, a tonic phase of about 10 to 30 seconds with rigidity, clenched jaw, apnoea and cyanosis, a clonic phase of 1 to 2 minutes with rhythmic jerking and frothing at the mouth, and a post-ictal phase of 5 to 30 minutes of deep sleep, confusion, headache and muscle ache.
Lateral tongue biting, urinary and occasionally faecal incontinence and a post-ictal confusion support a true tonic-clonic seizure; a transient focal weakness afterwards is Todd paresis and resolves within hours.
During the seizure: stay with the patient and call for help, note the exact time of onset, ease the patient to the floor if standing, cushion the head, remove spectacles, loosen tight clothing at the neck, clear away hard objects and furniture, and provide privacy by screening the bed.
Never restrain the limbs, never force anything between the teeth, never try to open the jaw or insert an oral airway during the convulsion, and give nothing by mouth until the patient is fully awake — these are the four errors examined most often, and forcing an object into the mouth breaks teeth and obstructs the airway.
As soon as the jerking allows, turn the patient into the left lateral recovery position so that saliva and vomit drain, keep suction and oxygen ready at the bedside, and give oxygen once the airway is clear.
A convulsion that lasts 5 minutes or more, or a second seizure before consciousness returns, is status epilepticus and needs the emergency drug protocol — check the capillary glucose, secure intravenous access and give the prescribed benzodiazepine while calling for help.
Afterwards: maintain the airway, suction secretions, check vital signs, oxygen saturation and capillary glucose, examine for injuries including tongue laceration, head injury and posterior shoulder dislocation, reorient the patient gently, allow sleep, and reassure and stay with them because fear and embarrassment are part of the event.
Documentation is part of the treatment and should record what the patient was doing beforehand, any aura, the time of onset and total duration, where the movements began and how they spread, eye and head deviation, colour change, incontinence, tongue biting, the duration and character of the post-ictal state and any injuries.
Ward seizure precautions are the bed kept low with the rails up and padded where policy allows, oxygen and suction checked at the bedside, no oral thermometers, supervised bathing with showers instead of tub baths, and intravenous access in high-risk patients.

Pontine haemorrhage

Pontine haemorrhage is bleeding into the pons, almost always from chronic hypertensive damage to the paramedian perforating branches of the basilar artery, and it accounts for roughly 5 to 10 per cent of intracerebral haemorrhages. It is the most lethal site of all because the pons contains the reticular activating system, the respiratory centres and every descending motor tract, so a small bleed produces deep coma within minutes.

The picture is abrupt and complete: sudden coma, pinpoint pupils of 1 to 2 mm that still react to light when viewed with a magnifier, quadriplegia progressing to decerebrate posturing, absent horizontal eye movements with ocular bobbing, hyperthermia and irregular apneustic or ataxic breathing.
Pinpoint pupils have three classic causes and the discriminator is what comes with them: opioid overdose has depressed respiration and reverses with naloxone, organophosphate poisoning has salivation, lacrimation, sweating, bronchorrhoea and fasciculations, and pontine haemorrhage has coma with quadriparesis and reactive pinpoint pupils.
A ventral pontine lesion can leave the patient locked in — quadriplegic and unable to speak but fully conscious, with vertical eye movements and blinking preserved — so speak to every such patient normally and establish a blink code rather than assuming unconsciousness.
Diagnosis is by immediate non-contrast computed tomography, which shows fresh blood at once; the prognosis worsens with a haematoma above about 5 mL or extending beyond 2 cm in diameter, with hyperthermia, and with extension into the fourth ventricle.
Management is supportive and there is no useful surgery for a pontine bleed, unlike a cerebellar haemorrhage over 3 cm which is evacuated: secure the airway and ventilate, lower the systolic blood pressure carefully to about 140 mmHg, reverse any anticoagulation, control fever and blood sugar, and admit to intensive care.
Nursing care is airway protection with regular suction, strict nil by mouth with early enteral feeding once the gut is usable, temperature control for central hyperthermia, eye care in the patient who cannot blink, two-hourly turning and pressure area care, and thromboprophylaxis.
Because mortality is very high, honest, early and repeated communication with the family, symptom control, and discussion of ceilings of treatment and of organ donation where appropriate are as much part of the plan as the monitoring.

Cessation of breathing — brain death criteria

Brain death, called brainstem death in Indian law, is the irreversible loss of all function of the brain including the brainstem, so that the patient cannot breathe and will never regain consciousness even though the heart continues to beat on a ventilator. It is a legal declaration of death, not a prognosis, and it is what makes withdrawal of ventilation and deceased-donor organ donation lawful under the Transplantation of Human Organs and Tissues Act, so the certification process is rigid, documented and never performed by a single doctor.

Prerequisites before any testing: a known, irreversible structural cause of coma on imaging; core temperature at or above 35 degrees Celsius; systolic blood pressure adequate for cerebral perfusion; no sedatives, opioids, neuromuscular blockers or alcohol still acting (checked against half-lives and, where available, drug levels or a nerve stimulator); and no severe metabolic, electrolyte or endocrine derangement that could explain the coma.
The clinical examination has three parts: deep coma with no response to painful stimulus in the cranial nerve distribution, absent brainstem reflexes, and a positive apnoea test.
Absent brainstem reflexes to be documented individually: pupillary light reflex (fixed, mid-position or dilated pupils), corneal reflex, oculocephalic (doll's eye) response, oculovestibular response to 50 mL of ice-cold water in each ear with the head at 30 degrees, gag reflex, cough reflex on deep tracheal suction, and absent facial movement to supraorbital pressure.
The apnoea test: pre-oxygenate with 100% oxygen, disconnect the ventilator while giving oxygen through a catheter in the trachea, and observe the chest and abdomen for about 8 to 10 minutes; the test is positive when there is no respiratory effort at all and the arterial carbon dioxide has risen to 60 mmHg or more, or by at least 20 mmHg above the baseline value.
The apnoea test is abandoned and the patient reconnected if the oxygen saturation falls below about 85%, if the blood pressure drops significantly or if arrhythmias appear; an ancillary test such as EEG or cerebral angiography is then used instead.
Under Indian law the declaration is made by a board of four registered medical practitioners — the medical practitioner in charge of the hospital, an independent practitioner nominated from the panel approved by the appropriate authority, a neurologist or neurosurgeon similarly nominated, and the doctor treating the patient — and the whole examination is repeated after an interval of 6 hours, with both sets recorded on the prescribed form.
Spinal reflexes may persist and can be dramatic — triple flexion of the legs, deep tendon reflexes, and the Lazarus sign in which the arms rise and cross the chest; these are generated below the foramen magnum and do not contradict brain death, and the family must be prepared for them.
The neurosurgeon or neurologist on the board and the doctor treating the patient must not be part of the transplant team, and the request for donation is made separately, by a trained transplant coordinator, only after the declaration is complete — the two conversations are deliberately decoupled.
Once brain death is declared, the time of death is the time of the second confirmatory examination; if organ donation proceeds, nursing care shifts to donor maintenance — mean arterial pressure and perfusion, normothermia with active warming, treatment of diabetes insipidus with desmopressin, lung-protective ventilation, glycaemic control and infection prevention.
Brain death is not a coma, not a persistent vegetative state and not the same as cardiac death; a vegetative patient breathes spontaneously and has brainstem reflexes, and that difference is the single most examinable point.

Kaposi sarcoma

Kaposi sarcoma is a multifocal vascular tumour of endothelial origin caused by human herpesvirus 8 (also called Kaposi sarcoma-associated herpesvirus) in a host whose immunity is impaired. In its AIDS-associated form it is an AIDS-defining, WHO stage 4 condition, and because the tumour is driven by immune failure rather than by cell autonomy, restoring immunity with antiretroviral therapy is itself the main treatment.

Four epidemiological forms: classic, an indolent disease of elderly men of Mediterranean and Eastern European origin affecting the lower legs; endemic African, which can be aggressive and lymphadenopathic in children; iatrogenic, in transplant recipients, which often regresses when immunosuppression is reduced or switched to an mTOR inhibitor such as sirolimus; and epidemic AIDS-associated, the aggressive disseminated form.
The lesions begin as painless violaceous, purple-brown or dark macules that become plaques and then firm nodules; they do not blanch on pressure, often follow skin tension lines, may be oval and elongated, and can ulcerate, bleed and cause disfiguring lymphoedema of the legs and face.
Distribution in the AIDS-associated form is widespread and includes the mucosa — the hard palate is a classic site — as well as the gastrointestinal tract, where it bleeds, and the lungs, where it causes breathlessness and haemoptysis and carries the worst prognosis.
Diagnosis is by skin or endoscopic biopsy showing spindle cells with slit-like vascular spaces, extravasated red cells and haemosiderin, confirmed with HHV-8 LANA immunostaining; a purple nodule in an HIV-positive patient is not assumed to be Kaposi sarcoma without it.
The key differential is bacillary angiomatosis caused by Bartonella, which looks similar but is a bacterial infection that resolves with erythromycin or doxycycline; the others are pyogenic granuloma, haemangioma, dermatofibroma and cutaneous lymphoma, and the biopsy is what separates them.
Treatment: antiretroviral therapy is the backbone and many limited lesions regress with immune reconstitution; localised disease is treated with radiotherapy, intralesional vinblastine, cryotherapy or excision; extensive cutaneous, visceral or pulmonary disease needs systemic chemotherapy, usually liposomal doxorubicin or paclitaxel.
Lesions may paradoxically flare in the first weeks of antiretroviral therapy as immune reconstitution inflammatory syndrome; this is reported and managed, not treated by stopping the antiretrovirals.
Nursing care is skin protection and dignity: handle fragile nodules gently, use non-adherent dressings on ulcerated or bleeding lesions, elevate and support lymphoedematous limbs with skin care and prescribed compression, manage pain, and address body image and the visible stigma of facial lesions.
Reassure the household that touching the lesions does not spread the tumour; HHV-8 spreads chiefly through saliva and sexual contact, and the tumour itself is not contagious by casual contact.
Prevention in practice is early HIV diagnosis and prompt antiretroviral therapy, because the incidence of Kaposi sarcoma falls sharply once CD4 counts are kept above 200.

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