Neurology Flashcards

Question

What is the aetiology of ischaemic stroke?

Answer 1

Cardiac: - Atherosclerotic disease: smoking, hypertension, diabetes, high cholesterol - Atrial fibrillation Vascular: - Aortic dissection - Vasculitides Haematological: - Hypercoagulability e.g. antiphospholipid syndrome - Sickle cell disease

Answer 2

Intracerebral - Trauma - Hypertension Subarachnoid - Berry aneurysm Extradural and subdural haemorrhages are not considered haemorrhagic strokes.

Answer 3

In neurology, suspect a vascular cause when there is a sudden onset of neurological symptoms. Stoke symptoms are typically asymmetrical: Sudden weakness of limbs Sudden facial weakness Sudden onset dysphasia (speech disturbance) Sudden onset visual or sensory loss

Answer 4

Contralateral hemiparesis (weakness of one side of the body) and sensory loss with lower limbs > upper limbs

Answer 5

- Contralateral hemiparesis and sensory loss with upper limbs > lower limbs - Homonymous hemianopia - Aphasia: if affecting the ‘dominant’ hemisphere (the left in 95% of right-handed people) - Hemineglect syndrome: if affecting the ‘non-dominant’ hemisphere - unaware and ignoring non-dominant side

Answer 6

Posterior cerebral artery - Contralateral homonymous hemianopia with macular sparing (due to dual blood supply from MCA and PCA to macula) - Visual agnosia (inability to recognize objects, persons, sounds, shapes, or smells)

Answer 7

1) Cerebellar signs - Dysdiadochokinesia - Ataxia (gait and posture) - Nystagmus - Intention tremor - Slurred speech - Hypotonia/heel-shin test 2) Reduced consciousness 3) Quadriplegia or hemiplegia

Answer 8

Amaurosis fugax - temporary loss of vision in one or both eyes due to loss of blood flow to the retina

Answer 9

"Locked-in" syndrome

Answer 10

Midbrain infarct - affecting branches of the PCA. Clinical presentation: - Oculomotor palsy and contralateral hemiplegia

Answer 11

- 1st line: non-contrast CT head: usually normal in the first few hours of ischaemic stroke but hyperdense blood if haemorrhage - ECG: assess for atrial fibrillation - Bloods: screens Hba1c, lipids, clotting screens. Helps exclude mimics such as hypoglycemia and hyponatraemia

Answer 12

Conservative: maintain glucose level, hydration and temp Antiplatelet: - Aspirin 300 mg: ASAP after haemorrhage is excluded on CT - If thrombolysis, start aspirin 24 hours after once haemorrhage is excluded Thrombolysis (meds to dissolve clot): - If < 4.5 hours of symptom onset (less effective after window) and haemorrhage excluded on imaging Thrombectomy (surgery to remove clot): - Confirmation of stroke using CTA (CT of blood vessels) or MR angiogram before thrombectomy Anticoagulation: - If AF is the cause - anticoagulation should only be started >14 days post-stroke. Aspirin 300 mg until then.

Answer 13

- 1st line: clopidogrel 75 mg daily lifelong is (after two weeks of aspirin) - High-dose statin: e.g. atorvastatin 20-80mg, usually after 48 hours of the stroke - Manage hypertension, diabetes, smoking and other cardiovascular risk factors

Answer 14

Depends on the subtype. - Subarachnoid haemorrhage usually requires endovascular or surgical clipping. - Admit to neurocritical care: intensive monitoring due to the risk of raised intracranial pressure and airway compromise. - ICP: consider intubation with hyperventilation, head elevation (30°) and IV hypertonic saline/mannitol. - Surgical intervention: decompression may be needed - treats compressed nerves

Answer 15

Ramipril - beta-blocker Atorvastatin - statin

Answer 16

Transient ischaemic attack (TIA) refers to a period of transient cerebral ischemia resulting in a self-resolving neurological deficit within 24 hours. Stroke features > 24 hours

Answer 17

Definition of TIA moving from time-based to tissue-based: A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.

Answer 18

Similar to the aetiology of ischaemic stroke, usually caused by thromboembolic disease

Answer 19

~ 15% of patients have at least one TIA before a stroke. - Increasing age - Hypertension - Smoking - Diabetes - Hypercholesterolaemia - Atrial fibrillation - Carotid stenosis

Answer 20

Symptoms - Facial weakness - Limb weakness - Slurred speech - Amaurosis fugax: a painless temporary loss of vision, usually in one eye Signs: - Focal neurology on examination (signs specific to affected brain area) - Irregular pulse: suggests atrial fibrillation as an underlying cause - Carotid bruit (heart sound due to turbulent, non-laminar flow): suggests carotid artery stenosis

Answer 21

ECG: rule out atrial fibrillation as an underlying cause Bloods: screen for Hba1c, lipids, clotting screen and rule out hypoglycemia and hyponatraemia (mimics TIA) TIA clinic: most recent guidance states that all patients should be seen within 24 hours of symptom onset At the TIA clinic: - Specialist assessment - MRI head - Carotid doppler (USS - images of big arteries in the neck that supply the brain).

Answer 22

Acute: 1st line: antiplatelet: initially aspirin 300mg - until the patient is reviewed in TIA clinic. Do not offer aspirin if: Bleeding disorder or taking an anticoagulant: needs immediate admission and assessment - Carotid endarterectomy (removal of fatty plaques from carotid arteries): stenosis of > 70% on Doppler = urgent endarterectomy

Answer 23

1. 1st line: Clopidogrel 75 mg daily once the patient has been reviewed in TIA clinic and the diagnosis confirmed 2. High-dose statin: all patients e.g. atorvastatin 20-80mg 3. Manage hypertension, diabetes, smoking and other cardiovascular risk factors

Answer 24

- Type of haemorrhagic stroke, and thought to be caused by damage to small cerebral vessels, which results in bleeding into the brain tissue.

Answer 25

- Hypertension (most common) - Older age - Male sex - Asian, black and/or Hispanic - Illicit drug use e.g. cocaine - FHx of ICH

Answer 26

- Unilateral weakness or paralysis in the face, arm, or leg - Sensory loss (numbness) - Dysphasia - Dysarthria (inability to control speech muscles) - Visual disturbance - Photophobia - Headache - Ataxia (impaired movement coordination)

Answer 27

- Non-contrast CT head - hyperdense area due to bleed - Serum glucose to rule out hypo and hyperglycemia as mimic - Serum electrolytes to rule out hyponatremia as cause for neurological symptoms - Serum urea and creatinine to rule out renal failure as contraindicated in some stroke treatments - Liver function tests to rule out liver dysfunction as a cause of haemorrhage - FBC to rule out thrombocytopenia as the cause of haemorrhage - Clotting screen to rule out coagulopathy as the cause of haemorrhage - ECG - abnormal ECG can indicate myocardial injury

Answer 28

Suspected ICH: - 1st line: Stabilisation using ABCDE, then refer to hyper-acute or acute stroke ward Confirmed ICH: - 1st line: supportive care and monitoring: - Assess GCS - Maintain SpO2 > 96% (>88% if at risk of hypercapnic resp failure) - Maintain stable BP + blood glucose - Neurosurgery referral assessment if suitable

Answer 29

Subarachnoid haemorrhage (SAH) is a type of haemorrhagic stroke, characterised by blood within the subarachnoid space. It is most commonly caused by trauma (traumatic SAH). Characteristic "thunderclap headache" - severe, sudden onset headache

Answer 30

Most common - trauma (traumatic SAH) Most non-traumatic cause - rupture of an intracranial aneurysm - accounts for 80% of cases: Berry aneurysm - arises at arterial bifurcation of the circle of Willis, most commonly in junction between anterior communicating and anterior cerebral arteries

Answer 31

Symptoms: - Headache - Severe, sudden onset - Occipital - ‘Thunderclap’ headache - Meningism: photophobia and neck stiffness - Nausea and vomiting - Confusion, coma and seizures Signs: - 3rd nerve palsy (oculomotor) - an aneurysm arising from the posterior communicating artery will press on the 3rd nerve, causing a palsy with a fixed dilated pupil. - 6th nerve palsy (abducens) - a non-specific sign which indicates raised intracranial pressure - Reduced GCS

Answer 32

The investigations below should be performed alongside basic blood tests, including serum glucose (hyperglycemia in 1/3 patients) and clotting screen (elevated INR + prolonged PTT). - Urgent non-contrast CT head: diagnostic - CT imaging typically shows blood in the basal cisterns - ECG: should be requested for all patients and may demonstrate arrhythmias, ischaemic and ST-elevation (can mimic acute coronary syndrome/STEMI)

Answer 33

1. Once SAH confirmed, refer immediately to neurosurgery 2. Intervention should be performed within 24 hours due to the risk of rebleeding. 3. 1st line: nimodipine give immediately upon diagnosis, prevents vasospasm - 21-day course 4. Intervention: 1st line is endovascular coiling of the aneurysm 4. If features of raised intracranial pressure: consider intubation with hyperventilation, head elevation (30°) and IV mannitol 6. Conservative: - Bed rest - Antitussive agent (anti-cold meds) and stool softeners: prevents straining and therefore reduce the risk of rebleeding

Answer 34

An extradural haemorrhage (also known as an ‘epidural’ haemorrhage) is bleeding into the potential space between the skull and the dura mater. The blood then collects in this space and is referred to as an extradural haematoma (EDH). Not a stroke!

Answer 35

EDH is usually caused by trauma, e.g. blunt trauma to the head: Arterial bleeding: the majority of EDHs occur as a result of rupture of the middle meningeal artery.

Answer 36

The exact presentation varies based on injury location, and most patients have skull fractures: 1. Initial loss of consciousness 2. Lucid interval in about 20% patients, regains full consciousness due to venous shunting of blood 3. Worsening neurological status: - Local compression due to haematoma expansion = brain herniation - Reduced GCS - Cushing’s reflex: hypertension, irregular breathing and bradycardia - Nausea and vomiting 4. Evidence of head injury: - Bruising or scalp haematoma - Battle’s sign (bruising behind the mastoid process - behind the ear) - Periorbital haematoma (Racoon eyes)

Answer 37

Primary investigations: Non-contrast CT head: hyperdense well-demarcated biconvex collection below the temporal bone, and the bleed should be limited by the cranial sutures - Can also assess for skull fracture: - Features of mass effect (not the video game but effect exerted by any mass, presenting as a clinically significant haematoma), such as brain herniation

Answer 38

An urgent neurosurgical opinion is required. General principles aim to reduce/control intracranial pressure: 1. Bed position: have the head of the bed tilted up at ~30 degrees. 2. Intubation: if the patient has reduced GCS 3. Oxygen: ensure adequate oxygenation 4. IV hypertonic saline/mannitol = reduce ICP 5. Burr hole: temporising measure to reduce ICP before definitive management Definitive management: - Craniotomy and haematoma evacuation: - Indicated if the EDH is greater than 30cm3 - <30cm3 without focal deficit managed non-operatively with serial CT scanning and close neurological observation in a neurosurgical centre

Answer 39

A subdural haemorrhage occurs when blood accumulates between the dura and arachnoid mater (subdural space), forming a subdural haematoma (SDH) collection. Not a stroke!

Answer 40

Subdural haemorrhage commonly occurs after trauma. The subdural space contains bridging veins which take blood from the brain to the dural venous sinuses. If these veins rupture, they can bleed into the subdural space.

Answer 41

Classified in terms of acuity: 1. Acute SDH are < 3 days old - Caused by traumatic rupture of bridging cortical veins 2. Chronic SDH are > 21 days old - Caused by traumatic rupture of bridging cortical veins Usually associated with cortical atrophy e.g. elderly and alcoholics > cortical veins more prone to rupture and require lower impact trauma Cortical atrophy results in larger subdural space, so haematomas can enlarge significantly over time while remaining asymptotic 3. Subacute SDH are 3-21 days

Answer 42

Symptom onset within 3 days of inciting event: - May have a lucid interval - Reduced consciousness - Headaches and vomiting - Slurred speech - Focal neurological deficit, e.g. weakness or fixed dilated pupil - Cushing’s reflex - hypertension, irregular breathing, bradycardia - Seizures

Answer 43

The Cushing reflex is a physiological nervous system response to acute elevations of intracranial pressure (ICP). This results in the Cushing triad of widened pulse pressure (increasing systolic, decreasing diastolic) (and hypertension), bradycardia, and irregular respirations.

Answer 44

- Insidious onset usually in the elderly or alcoholics Symptoms - Progressive confusion and cognitive deficit - Headaches and vomiting Signs - Focal neurological deficit, e.g. weakness or fixed dilated pupil

Answer 45

A classification system to assess a patient's level of impaired consciousness and coma Assess eye-opening, verbal and motor response. Severe Head Injury = GCS score of 8 or less Moderate Head Injury = GCS score of 9 to 12 Mild Head Injury = GCS score of 13 to 15

Answer 46

Primary investigations: - Non-contrast CT head: SDH appears as a crescentic collection around the surface of the brain which is not limited by the suture lines of the skull unlike in an extradural haemorrhage. There may be evidence of mass effect such as midline shift or herniation - Acute: hyperdense (bright) - Subacute: as the clot matures, the density starts to drop until it is isodense to the brain cortex - Chronic: becomes hypodense (dark)

Answer 47

General principles - aim to reduce/control intracranial pressure: 1. **Bed position:** have the head of the bed tilted up at ~30 degrees 2. **Intubation:** if the patient has reduced GCS 3. **Oxygen:** ensure adequate oxygenation Maintain adequate cerebral perfusion (Perfusion = MAP - ICP) 4. **Inotropes and vasopressors** 7. **Fluids** 8. **Osmotherapy:** hypertonic saline or mannitol helps shift extracellular fluid and CSF into the vascular compartment, reducing ICP 9. **Burr hole (holes in skull):** temporising measure to reduce ICP prior to definitive management

Answer 48

Definitive management: Conservative: observation for small acute and chronic SDHs not causing neurological deficits Surgery: involves craniotomy and evacuation. Indications for acute SDH are as follows: - Acute SDH with a thickness > 10mm or a midline shift > 5mm - GCS < 9 and continuing decrease - Fixed and dilated pupils - ICP > 20 mmHg Chronic SDH = surgical evacuation because of mass effect and symptoms

Answer 49

Meningitis describes inflammation of the leptomeninges (arachnoid and pia mater) and usually occurs due to a bacterial, viral, or fungal infection. Bacterial meningitis = acute emergency!

Answer 50

The cause can be bacterial, viral or fungal. It can also be caused by trauma, cancer or drugs. Bacterial: The most common causes are N. meningitidis and S. pneumoniae in the UK Viral: Enteroviruses such as coxsackievirus are the most common cause. Fungal meningitis: - Cryptococcus neoformans - Candida -Mainly affects immunocompromised patients, very rare in immunocompetent people

Answer 51

1) 0 to 3 months: Group B streptococcus* E. coli Listeria monocytogenes 2) 3 months to 6 years: Neisseria meningitidis Streptococcus pneumoniae Haemophilus influenzae 3) 6 months to 60 years: Neisseria meningitidis Streptococcus pneumoniae 4) > 60 years: Streptococcus pneumoniae Neisseria meningitidis Listeria monocytogenes

Answer 52

- Immunocompromised: children, elderly, HIV patients, chemo patients. - Non-immunised: at risk of H. influenza, pneumococcal and meningococcal meningitis - Crowded environment: e.g. students living in halls of residence

Answer 53

Symptoms: 1. Meningism - Headache - Photophobia - Neck stiffness 2. Fever 3. Nausea and vomiting 4. Seizures Signs: 1. Kernig’s sign: when the hip is flexed and the knee is at 90°, extension of the knee results in pain 2. Brudzinski sign: severe neck stiffness causes the hips and knees to flex when the neck is flexed 3. Petechial or purpuric non-blanching rash: associated with meningococcal disease (N. meningitidis) 4. Pyrexia 5. Reduced GCS

Answer 54

1) 1st line: Blood cultures: positive in the case of bacterial infection 2) Gold standard: Lumbar puncture (CSF sample taken from L3- L4 and sent for bacterial culture and viral PCR) + CSF analysis. - CSF gram stain: S. pneumoniae (gram-positive cocci in chains); N. meningitidis (gram-negative diplococci) - CSF culture - CSF PCR: useful for viruses such as HSV and VZV (varicella aka chickenpox) 3. FBC: leukocytosis 4. CRP: raised inflammatory markers 5. Blood glucose: required in all patients and for comparison with CSF glucose

Answer 55

NICE guidelines state not to perform an LP without consultant instruction if any of the following contraindications are present: - Raised intracranial pressure suspected (e.g. papilloedema) - Reduced or fluctuating consciousness (GCS < 9 or a drop of ≥ 3) - Relative bradycardia and hypertension - Focal neurological signs - Dilated pupil - Shock - After convulsions (until stabilised) - Coagulation abnormalities, platelet count <100x109/L or on anticoagulants - Local infection at the lumbar puncture site

Answer 56

- SAH (subarachnoid haemorrhage) - Migraine - Encephalitis - Flu

Answer 57

1) Empirical therapy = IV cefotaxime (+ amoxicillin if < 3 months or >50 years) 2) Assess GCS 3) Antibiotics for most common bacterial causes: - N. meningitidis - IV benzylpenicillin (or cefotaxime) - S. pneumonia - IV cefotaxime - Haemophilus influenzae meningitis - IV cefotaxime 4) Viral = Acyclovir

Answer 58

People with close, prolonged contact with patients with meningococcal infections (such as meningitis or septicaemia). The risk of contracting illness highest within 7 days before the onset of illness and within 7 days after diagnosis. 1st line treatment: single dose 500mg oral ciprofloxacin

Answer 59

Appearance = Cloudy Protein = High (>1g/L) Glucose = Low (<50% serum glucose) White Cell Count = High - 10-5000/mm3 (neutrophils) Culture = Bacteria Remember! Interpreting lumbar puncture results is a common exam question. Bacteria in CSF = release of protein + use up glucose. Viruses don’t use glucose but release small amounts of protein. The immune system releases neutrophils in response to bacteria and lymphocytes in response to viruses.

Answer 60

Appearance = Clear Protein = Mildly raised/normal (<1g/L) Glucose = High (>60% serum glucose) White Cell Count = High 1000/mm3 (lymphocytes) Culture = Negative Remember! LP interpretation = common exam q! Viruses don't use glucose and may release only a small amount of protein. Immune system will release lymphocytes in response to viruses

Answer 61

Multiple sclerosis (MS) is an autoimmune, cell-mediated demyelinating disease of the central nervous system.

Answer 62

- Age: most commonly diagnosed in 20-40-year-olds - Female gender: x3 more women affected - Northern latitudes - Vitamin D deficiency - Family history: HLA-DR2 is implicated; 30% monozygotic twin concordance - Family history of other autoimmune disorders - EBV infection

Answer 63

Unclear aetiology but thought to be an interplay between environmental triggers and genetic susceptibility, comprising an inflammatory and degenerative component. Various factors have been implicated, including infection with EBV, vitamin D deficiency, and HLA association.

Answer 64

1. Relapsing-remitting: - The most common pattern (85% of cases) Episodic flare-ups (may last days, weeks or months), separated by periods of remission. - 60% of patients develop secondary progressive MS within 15 years 2. Secondary progressive: - Starts with relapsing-remitting course, but symptoms progressively worse with no periods of remission - coordination difficulties, bowel/bladder problems 3. Primary progressive: - 10% patients and common in older patients - Symptoms get progressively worse from disease onset with no periods of remission.

Answer 65

Symptoms: - Blurred vision and red desaturation: optic neuritis (swelling that damages the optic nerve) is the most common presenting feature - Numbness, tingling and other strange sensations - Weakness - Bowel and bladder dysfunction - Uhtoff’s phenomenon: worsening of symptoms following a rise in temperature, such as a hot bath

Answer 66

Signs: 1. Visual: optic neuritis 2. Sensory loss: due to demyelination of spinothalamic or dorsal columns 3. Upper motor neuron signs with spastic (increased muscle tone) paraparesis are common 4. Cerebellar signs: such as ataxia and tremor (usually in a relapse) 5. Lhermitte’s phenomenon: electric shock sensation on neck flexion

Answer 67

1. MRI brain and spine: Demyelinating plaques: Dawson’s fingers, perpendicular to the lateral ventricles > suggestive of MS 2. Diagnostic MRI brain and spine + McDonald's criteria (≥ 2 relapses) Old lesions will not enhance with contrast, whereas newer lesions will. This provides evidence of the dissemination of lesions in time (separate events) and space (different parts of CNS affected), which is required for a diagnosis of MS - Lumbar puncture: oligoclonal bands found in the CSF and not in the serum (unmatched), indicating increased IgG.

Answer 68

1. Relapse: - Steroids: reduce relapse duration,1st line: oral or IV methylprednisolone for 5 days 2) Maintenance therapy: reduce the relapse rate, for patients 2 relapses in 2 years or progression on MRI 1st line disease-modifying drugs: - Beta-interferon: reduces relapse rate, but not progression - Glatiramer acetate: immunomodulator drug which might kill immune cells that attack myelin

Answer 69

Guillain-Barré syndrome (GBS) is an autoimmune, rapidly progressive demyelinating condition of the peripheral nervous system, often triggered by infection.

Answer 70

GBS is believed to be caused by ‘molecular mimicry.’ A pathogenic antigen (e.g. Campylobacter jejuni) resembles myelin gangliosides in the PNS. The immune system targets the antigen and attacks the myelin sheath of sensory and motor nerves. This autoimmune process involves the production of anti-ganglioside antibodies (anti-GMI +ve 25% of patients)

Answer 71

1) Acute inflammatory demyelinating polyneuropathy (ADIP): ~90% of cases

Answer 72

- Myasthenia Gravis - Polymyositis

Answer 73

Typical presentation - symmetrical muscle weakness affecting lower extremities before upper (ascending weakness). History of infection within the preceding 6 weeks Subacute, with peak symptoms within 2-3 weeks of disease onset

Answer 74

Signs: - Reduced sensation in affected limbs - mild on examination - Symmetrical weakness in lower extremities first, progressing to the upper limbs: proximal muscles affected before distal muscle - Ataxia with hyporeflexia (or areflexia - absent deep tendon reflexes) in affected limbs

Answer 75

Mainly a clinical diagnosis - progressive weakness and areflexia/hyporeflexia in weaker limbs. - Diagnostic lumbar puncture: raised CSF protein with normal WBC count is typical - Nerve conduction studies - suggestive of demylintion e.g. reduced conduction velocity - LFTs: raised AST (aspartate aminotransferase) and ALT (alanine aminotransferase) - Spirometry: shows reduced vital capacity + used to monitor respiratory function

Answer 76

1st line: IV immunoglobulins (IVIg): 5 day treatment course started within 2 weeks of symptom onset OR Plasma exchange - over 2 weeks within 4 weeks of symptom onset

Answer 77

Parkinson’s Disease (PD) is a neurodegenerative disorder characterised by loss of dopaminergic neurones within the substantia nigra pars compacta (SNPC) of the basal ganglia (nigrostriatal pathway).

Answer 78

Idiopathic, aetiology not clear. Key genes involved are abnormalities in those that code for α-synuclein and the ubiquitin-protease system. This results in a loss of transmission between the basal ganglia, thalamus, and motor cortex, resulting in impaired control of voluntary movements.

Answer 79

Histological hallmark - eosinophilic inclusion bodies (Lewy bodies) consisting of misfolded α-synuclein in the dopaminergic neurones The effect of these misfolded proteins is still unclear but thought that misfolded α-synuclein may spread to neighbouring brain regions in a prion-like fashion

Answer 80

Parkinson’s Disease is the second most common neurodegenerative disease (after Alzheimer’s Disease): - Age: prevalence of 1% in 60-70 and around 1-3% in ≥80 - Gender: males are x1.5 more likely to develop PD - Family History

Answer 81

Parkinsonism: - Bradykinesia - Tremor (resting 3.5Hz, distal, reduce on action) - Rigidity - Postural instability (causing shuffling gait with short, rapid steps (festination)) Non-motor symptoms: - Anosmia - Sleep disturbance - Psychiatric symptoms including: depression, anxiety, dementia - Constipation

Answer 82

- Lewy-body dementia (if dementia symptoms onset before parkinsonism) - Wilson's disease - Meds (e.g. antipsychotics) - CNS infections - following encephalitis

Answer 83

1. 1st line - Mainly clinical diagnosis for typically presenting patients 2. Investigations to consider if atypical features or unclear clinical diagnosis - MRI brain: may help exclude other causes of neurological disease but should not be used to diagnose PD - SPECT (DaT scan): single-photon emission computed tomography (SPECT) will show reduced dopamine uptake in the basal ganglia

Answer 84

NICE recommends that patients with suspected PD should be referred to a specialist in movement disorders (either a neurologist or elderly care physician) for a diagnosis to be made. - Confirmed diagnosis should be reviewed every 6-12 months 1st line: 1. Motor symptoms affecting quality of life: - Levodopa (dopamine replacement) + decarboxylase inhibitor e.g. Co-beneldopa (combo reduces/stops N+V caused by Levodopa) 2. Motor symptoms not affecting quality of life - A choice of one of the following: - Dopamine agonist: e.g. ropinirole - Monoamine oxidase B inhibitor: e.g. selegiline - Levodopa + decarboxylase inhibitor Co-beneldopa

Answer 85

Progressive neurodegenerative disorder with 100% penetrance (proportion of carriers of a gene exhibiting an associated phenotype). It is an autosomal dominant, trinucleotide repeat disorder caused by a loss of the main inhibitory neurotransmitter GABA.

Answer 86

Huntington's disease is a trinucleotide repeat disorder caused by mutation in the huntingtin (HTT) gene (on chromosome 4), causing expanded CAG repeats at the N-terminus of the gene that codes for the huntingtin protein. CAG = glutamine ≤35 CAG repeats = normal 36 - 39 CAG repeats = reduced penetrance ≥40 CAG repeats = certain disease development Average age of onset around 40, but depends on number of CAG repeats

Answer 87

The polyglutamine tail on the HTT protein is cleaved and forms toxic fragments > causing neuronal cell death in the putamen and caudate nuclei (dorsal striatum) of basal ganglia, which have a role in movement inhibition and rely on GABA as its main neurotransmitter. Results in loss of GABA > less regulation of dopamine > excess dopamine > symptoms of Huntington's (see signs and symptoms card)

Answer 88

- Chorea - jerky, dance-like movements - Dystonia - muscle spasms and contractions - Incoordination - Cognitive and behavioural difficulties - Irritability, agitation and anxiety

Answer 89

Anticipation is a phenomenon in which the signs and symptoms of some genetic conditions tend to become more severe and/or appear at an earlier age as it is passed from one generation to the next. In terms of HD, the repeat expansion of CAG also affects DNA replication, with CAG repeats added during DNA replication. The greater the number of repeats, the more severe the disease. This affects sperm more so than eggs, This means the child of a parent with HD can inherit even more CAG repeats than the parent did > earlier age of symptoms onset, this is anticipation > HD manifest earlier with each generation

Answer 90

1. Clinical diagnosis 2. Diagnosis confirmation = CAG repeat test: - A positive result is ≥40 CAG repeats on 1 of the 2 alleles; an intermediate result is 36 to 39 repeats 3. MRI/CT = loss of striatal volume/striatal atrophy

Answer 91

1. 1st line is counselling for patients and family 2. Benzodiazepines, dopamine-depleting agents (e.g. tetrabenazine), antipsychotics (e.g. haloperidol) for chorea 3. SSRI for depression

Answer 92

Sydenham’s chorea ( Rheumatic fever)

Answer 93

- Poor prognosis - death within 10 - 20 years of diagnosis The most common cause of death = aspiration pneumonia Second most common cause = suicide

Answer 94

Encephalitis describes inflammation of the brain parenchyma.

Answer 95

The most common cause of encephalitis is herpes simplex virus-1 (HSV-1; 95% of cases), which causes temporal and inferior frontal lobe encephalitis. Other causes: - EBV - CMV - HIV - TB - Toxoplasmosis (close contact with cats)

Answer 96

- Immunocompromise (elderly, babies, HIV) - Blood/fluid exposure: HIV and West Nile virus - Mosquito bite: West Nile virus - Transfusion and transplantation: CMV, EBV, HIV - Close contact with cats: toxoplasmosis

Answer 97

Symptoms: 1. Fever 2. Headache 3. Behavioural changes: - Memory disturbance - Psychotic behaviour - Withdrawal or change in personality 5. Seizures Signs: 1. Pyrexia 2. Reduced GCS 3. Focal neurological deficit, such as: - Aphasia - Hemiparesis (weakness of one side of the body) - Cerebellar signs

Answer 98

Blood tests: FBC (high WBC count), CRP, U&Es (hyponatremia) and blood culture (can detect bacterial infection) Throat swab: culture for viral organisms CT or MRI (preferred) head: inflammation in the temporal and inferior frontal lobes in HSV encephalitis CSF analysis: lymphocytosis (high lymphocyte) with raised protein in the case of viral aetiology PCR: assays for common viral infections including HSV

Answer 99

Antiviral medication: Aciclovir - empirical treatment in all patients with suspected encephalitis caused by HSV-1

Answer 100

Dementia, is a progressive decline in cognitive function affecting multiple domains, including language, executive function, memory and social cognition

Answer 101

1. Alzheimer’s Disease (50-75%) 2. Vascular Dementia (up to 20%) 3. Dementia with Lewy-Bodies (10-15%) 4. Frontotemporal Dementia (2%)

Answer 102

Deposition of extracellular 𝛃-amyloid (senile plaques) and intracellular tau protein (neurofibrillary tangles) lead to neurotoxicity and reduced cholinergic transmission.

Answer 103

Reduced blood flow to the brain, secondary to small or large vessel disease.

Answer 104

Cortical and subcortical deposition of Lewy-Bodies (intracellular aggregates of ɑ-synuclein)

Answer 105

The progressive degeneration of the frontal and/or temporal lobes. associated with Pick bodies, with several subtypes such as Pick’s disease (build-up of tau proteins in neurons, accumulating into silver-staining, spherical aggregations i.e. Pick bodies)

Answer 106

- Age: risk increases with age - High BMI - increased inflammatory processes - Smoking: results in vascular changes as well as inflammation and oxidative stress - Type 2 diabetes: vascular changes - Hypertension: vascular changes - Depression - Low education - Hearing loss: from reduced cognitive stimulation - Social isolation and loneliness: reduced cognitive stimulation, and associated with poorer health outcomes

Answer 107

- Characteristic order of language impairment: naming → comprehension → fluency - Memory impairment

Answer 108

- Evidence of previous stroke - Depression and delusions - Emotional lability - Memory impairment - Gait disturbance and incontinence are sometimes seen.

Answer 109

- Cognitive symptoms precede motor symptoms unlike in Parkinson’s related dementia - Visual hallucinations and delusions - REM sleep disorder - Memory and attention impairment - Parkinsonism

Answer 110

- Behavioural and personality changes, e.g. impulsivity - Memory impairment - Language impairment e.g. reduced fluency or comprehension - develop a lot quicker than other forms

Answer 111

No specific tests for dementia, so investigations can focus on two factors to guide diagnosis: 1) Observing a change in behaviour over a period of time using: - History: incorporate cognitive, behavioural and psychological symptoms and impact on daily life - Cognitive assessments using a validated tool Most common: Folstein Mini-Mental State Examination (MMSE) - 11 questions testing orientation, attention, memory, language and visual-spatial skills A score of <24 out of 30 = abnormal 21 - 25 = reevaluation in 3 - 6 months MMSE should be combined with history and decline from the baseline level of functioning, as it might not detect mild cognitive decline. 2) Excluding reversible causes of cognitive decline: - Medication review: anticholinergics, opioids, benzodiazepines - Bloods: FBC (anaemia), U&Es (abnormal Na, Ca, glucose levels), TFTs (hypo/hyperthyroid), vitamin B12 (pernicious anaemia) - CT or MRI head to exclude a structural lesion

Answer 112

- Memory service: MDT involved in diagnosing and supporting patients - Education: education about dementia and adapting to changes - Advanced care plan: power of attorney, advanced statement on patient’s wishes, preferences to place of care and death - Cognitive stimulation therapy: activities and discussions aimed at improving cognitive and social functioning - Group reminiscence therapy: uses objects from daily life to stimulate memory and enable people to value their experiences. - Medication review

Answer 113

Mild/moderate disease: 1st line: AChE (Acetylcholinesterase) inhibitors: e.g. donepezil Moderate/severe disease: Memantine: NMDA receptor (glutamate as excitory neurotransmitter) antagonist in combination with an AChE inhibitor (but can be monotherapy if the former isn't tolerated)

Answer 114

1. Optimise cardiovascular risk factors: to reduce the likelihood of further ischaemic events 2. AChE inhibitor or memantine (glutamate receptor antagonist): if there is suspected comorbid Alzheimer’s disease, Dementia with Lewy-Bodies or Parkinson’s disease

Answer 115

1st line: AChE (Acetylcholinesterase) inhibitor: donepezil or rivastigmine Dopamine replacement (levodopa and carbidopa): if there is evidence of parkinsonism Atypical antipsychotics if severe psychiatric symptoms, but might worsen motor symptoms (avoid as far as possible)

Answer 116

- AChE inhibitors and memantine are not recommended - Conservative measures is recommended (see conservative management plan for dementia)

Answer 117

- Migraines - Tension headaches - Cluster headaches

Answer 118

- Giant cell/temporal arteritis - Thunderclap headache (subarachnoid haemorrhage) - Trauma - Medication overuse - Trigeminal neuralgia - Systemic infection - Meningitis/encephalitis

Answer 119

- Worst headache ever - New onset headache > 50 - Severe, quick onset - Abnormal pattern of migraine - Progressive or persistent headaches, or headaches that have changed dramatically

Answer 120

Migraine is a primary headache of complex aetiology which is usually episodic. ‘Classic' migraines are preceded by an aura, however, these only occur in one-third of patients.

Answer 121

- Migraine with typical aura - Migraine with atypical aura - Hemiplegic migraine - Silent migraine (migraine with aura but without a headache)

Answer 122

Triggers: CHOCOLATE - CHocolate - Oral Contraceptive - Alcohol + Anxiety - Travel - Exercise - Other important triggers include tiredness, lack of food, dehydration, menstruation, red wine and bright lights

Answer 123

- Neuronal hyperexcitability > trigeminal nerves initiates an inflammatory response > dilation of meningeal blood vessels, and sensitisation of surrounding nerve fibres = pain - The aura is thought to occur due to cortical spreading depression, a wave of depolarisation across the cerebral cortex.

Answer 124

1. Prodrome (days prior attack) Yawning, cravings, mood and sleep changes 2. Aura (typical or atypical) - before an attack 3. Clinical presentation - Unilateral pain but can be bilateral - Throbbing/pounding pain - Moderate to severe intensity - Nausea/ vomiting - Photophobia + phonophobia

Answer 125

Develops over 5 minutes, lasts 5-60 minutes and is fully reversible - Visual disturbances ( lines, dots, zigzags) - Somatosensory ( Paraesthesia, pins and needles) - Speech disturbances

Answer 126

May last more than 60 minutes - Motor weakness (e.g. hemiplegic migraine) - Diplopia - Visual symptoms affecting one eye - Poor balance (e.g. vestibular migraine) - Decreased level of consciousness Need urgent investigation to to rule out other sinister causes such as a stroke. Particularly for hemiplegic migraine, where patients can present with unilateral weakness and headache and can therefore easily be mistaken for a stroke.

Answer 127

Diagnosis is based on history and physical examination. No laboratory or imaging tests are essential for diagnosis. The diagnostic criteria is the International Classification of Headache Disorders (ICHD)-3 criteria for migraine.

Answer 128

1. Conservative management: avoid triggers 2. Acute: - Analgesia: ibuprofen or aspirin (900mg) or paracetamol - Mild: analgesia - Severe = oral triptans and analgesia e.g sumatriptan is 1st line - Antiemetic: metoclopramide 3) Chronic: - Headache diary - Avoid triggers - Prophylaxis - Propranolol is considered first-line 4) Prophylaxis (non-pharmacological): - Mindfulness - Acupuncture - Riboflavin (B2): may be effective in some people but avoid in pregnancy

Answer 129

Most chronic and recurrent daily headache, Most common primary headache. Classically they produce a mild ache across the forehead and in a band-like pattern around the head. Tension headaches comes on and resolve gradually and don’t produce visual changes.

Answer 130

- Missed meals - Conflict - Stress - Clenched jaw - Overexertion - Fatigue - Depression - Stress - Bad posture - Hunger - Noise

Answer 131

- Bilateral, pressing headache ( tight band) - Not aggravated by movement - 30 mins to 7 days - No nausea + vomiting - No more than one out of photophobia / phonophobia - Scalp tenderness

Answer 132

- Migraine - Cluster headache - GCA (giant cell arthritis) - Drug-induced headache ( worsens on analgesia

Answer 133

- Reassurance - Stress relief - Medication = Paracetamol , NSAIDs (Ibuprofen, diclofenac) - TCA’s - Analgesia no more than 6 days per month

Answer 134

- Cluster headache is an attack of severe pain localised to the unilateral orbital, supra-orbital, and/or temporal areas that lasts from 15 minutes to 3 hours. - It is the most painful and disabling primary headache. It is rare and more common in males - Onset between 20 and 40

Answer 135

- Male - Smoker - Alcohol - Genetics

Answer 136

- Rapid onset of excruciating pain generally localised around the eye - Unilateral rising to a crescendo over a few minutes and lasting between 15 to 160 mins, once or twice a day generally around the same time - Watery, bloodshot eye - Facial flushing - Rhinorrhoea - Miosis ( pupillary constriction ) / ptosis (droopy eyelid)

Answer 137

- Brain MRI - normal in primary cluster headaches, abnormal results might suggest secondary cause e.g. tumours. - ESR to exclude giant cell arteritis in patients over 50 years of age. Normal in primary cluster headaches - Pituitary function tests - normal in primary cluster headache; abnormalities may suggest secondary causes resulting from a pituitary adenoma - Diagnosis is based on the International Headache Society International Classification of Headache Disorders, 3rd edition (ICHD-3) criteria.

Answer 138

Acute 1) No analgesia 2) 1st line: 12L/min 100% oxygen for 15 mins via a non-rebreather mask (stops expired air going back into the oxygen reservoir) 3) Triptans - 1st line = Sumatriptan 4) Prophylaxis - 1st line = verapamil (CCB)

Answer 139

Trigeminal neuralgia is a pain syndrome which describes severe unilateral pain in the distribution of one or more trigeminal branches (ophthalmic, maxillary and mandibular zone)

Answer 140

90% of trigeminal neuralgia cases have compression of the trigeminal nerve typically by the superior cerebellar artery. Other causes include demyelinating disease (MS patients x20 more likely), posterior fossa masses, and brainstem infarcts.

Answer 141

- Advancing age: >40 - Female gender - Demyelinating disease: 20 times more common in patients with MS

Answer 142

Symptoms: As per NICE, the pain is as follows: - Trigeminal distribution (ophthalmic, maxillary and mandibular zones) - Severe - Unilateral - Electric shock-like sensation - Seconds to minutes - Episodic - Provoked, e.g. touch or cold - Some patients experience autonomic symptoms such as lacrimation, facial swelling, rhinorrhoea or ptosis Signs: - Pain may be provoked by touch on examination

Answer 143

Trigeminal neuralgia is a clinical diagnosis but further investigations may be considered to rule out alternative pathology. Consider: MRI brain: if a sinister cause is suspected e.g. space-occupying lesion or demyelination, or if the patient is refractory to medical treatment and surgery is being considered

Answer 144

1st line Medical: carbamazepine (anticovulasant) The dose is titrated upwards every 2 weeks until the pain is relieved. Refer to neurology: if there is severe pain or pain that significantly affects daily function, as well as patients refractory to treatment or with atypical symptoms (e.g. age < 50 years)

Answer 145

- Dental caries - Dental fracture - Mandibular osteomyelitis - Migraine

Answer 146

Epilepsy is a neurological disorder characterised by recurrent seizures. A seizure = paroxysmal alteration of neurological function resulting from the excessive, hypersynchronous discharge of neurons (a lot of neurons firing simultaneously) within the brain. Main excitatory neurotransmitter - glutamate, NMDA receptor The disrupted neurological function causing a seizure is the result of an imbalance between excitation and inhibition within the neurons of the brain.

Answer 147

Epilepsy can be inherited or acquired. Inherited: - Premature birth - Genetic condition: cerebral palsy: up to 30% have epilepsy etc. - Family history Acquired: - Traumatic brain injury - Neurodegenerative disease (Alzheimer's x10 more likely) - Ischaemic stroke - Intracerebral infection: meningitis - Illicit drug use: cocaine

Answer 148

- Focal: originates within one side of the brain, starting in the temporal lobes. - Generalised: involve both hemispheres of the brain at onset - Focal to bilateral: previously termed ‘secondary generalised’, the seizure starts on one side of the brain and spreads to both sides - Unknown: difficult to determine in some cases

Answer 149

- Motor - Non-motor - With retained awareness - Impaired awareness

Answer 150

Caused by distorted neuronal activity in the brain lobes involved in motor control (usually the frontal lobe). Symptoms include jerking, twitching or stiffening of a body part or automatisms such as licking lips, rubbing hands, walking

Answer 151

Seizures that cause changes in sensation, emotions, thinking or experiences

Answer 152

Focal seizures with retained awareness are when the patient is aware during the seizure, even if they cannot speak or respond

Answer 153

The patient is not aware when they are having a focal seizure

Answer 154

- Tonic-clonic - Tonic - Clonic - Myoclonic* - Atonic* - Generalised non-motor (absence) *Can be either generalised or focal

Answer 155

Stiffening of limbs (tonic) with rhythmic jerking (clonic) simultaneously (most people recognise this)

Answer 156

Sudden stiffness or tension in muscles of arm, legs or trunk.

Answer 157

Repeated jerking movements of arms or legs on one or both sides of the body.

Answer 158

Sudden, short-lasting jerks that can affect some or all of your body, usually lasts less than a second. Ranges from mild (a twitch) to forceful, which can cause the patient to throw things they are holding.

Answer 159

Sudden loss of muscle strength. Can cause a person to drop to the ground.

Answer 160

A seizure that involves brief changes in awareness - typically involves behavioural arrest or staring lasting 5 to 10 seconds

Answer 161

1) Temporal - memory, hearing and understanding language - hearing ringing/buzzing. Automatisms like lip-smacking, picking, walking 2) Frontal - motor control - twitching, jerking, stiffening of one part of your body 3) Parietal - spatial perception, touch, language understanding etc. - paraesthesia 4) Occipital - processing of visual info - visual hallucinations, transient blindness, rapid and forced blinking

Answer 162

Automatism: lip smacking, chewing, fumbling etc. Automatic behaviour: running, walking Auras: déjà vu, feeling of fear, unpleasant smells Auditory: buzzing, ringing, vertigo

Answer 163

Predominantly motor symptoms: thrashing, twitching, jerking

Answer 164

- Parasthesias - Visual hallucinations - Visual illusions

Answer 165

- Visual hallucinations - Transient blindness - Rapid and forced blinking - Movement of head or eyes to the opposite side

Answer 166

1) Prodrome - Precedes seizure by hours to days Weird feelings ( mood, behavioural changes) 2) Aura - Patient is aware + precedes other manifestations - Strange feelings in the gut, deja vu, strange smells, flashing lights - Can occur before a partial seizure 3) Ictal - seizure 4) Postictal - After seizure - Headache, confusion, myalgia, sore tongue ( often bitten) - Temporary weakness after focal seizure in motor cortex = Postictal Todd’s palsy - Dysphasia after temporal lobe seizure

Answer 167

Criteria for diagnosis: any one of the following: - 2 unprovoked seizures occurring > 24 hours apart - One unprovoked seizure + probability of future seizures e.g. abnormal EEG reading (> 60%) If the patient fulfills one of the above, then the epileptic syndrome diagnosis.

Answer 168

Electroencephalogram (EEG) - generalised epileptiform activity, or focal localising abnormality Investigations to exclude other causes. - Capillary blood glucose: to exclude hypo/hyperglycaemia as they can cause tonic-clonic seizures - FBC: leukocytosis could indicate CNS infection, which provoke generalised tonic-clonic seizures - U&Es - severe electrolyte imbalances (hyponatraemia, hypernatraemia, or uraemia) can cause generalised tonic-clonic seizures - Toxicology screen: if drug-induced seizure suspected - Imaging:CT head: to exclude intracranial causes such as haemorrhage All adults presenting with a seizure should be referred urgently to a specialist in the management of epilepsy (usually via a ‘first fit’ clinic) to ensure accurate and early diagnosis and initiation of appropriate therapy. DIagnosis by neurologist using combination of history and investigations.

Answer 169

Fever, hypoglycaemia or alcohol withdrawal. These "provoked" seizures above are caused by a specific substance/disease are reversible and do not fall under the diagnosis of epilepsy which is unprovoked.

Answer 170

Non-epileptic seizures: - Caused by fever, alcohol withdrawal, metabolic disturbances ( hyponatremia, hypoxia, hypoglycemia) - Lasts longer ( > 2 -3 mins), epileptic seizure ≤ 15s - Does not occur in sleep - No incontinence + tongue biting - No muscle pain

Answer 171

Conservative, medical or surgical Conservative: - Education: triggers to avoid, safety measures Stop driving: all patients must inform the DVLA: - First unprovoked seizure without structural abnormality or epileptiform activity on EEG: 6-month suspension - First unprovoked seizure with a structural abnormality or epileptiform activity on EEG: 12-month suspension

Answer 172

Anti-epileptic drugs (AEDs): - Generalised = sodium valproate (teratogenic - DO NOT PRESCRIBE to women who are able to have children) - Focal = lamotrigine or levetiracetam - Female of childbearing potential = Lamotrigine - Myoclonic = Levetiracetam / Topiramate - Absence = Ethosuximide

Answer 173

If medical management fails - Focal resection (removing brain tissue where the seizures originate) Lobe resection (removal of part of the temporal lobe) Lesionectomy: if a specific structural lesion is determined

Answer 174

A seizure is hypersynchronous, abnormal neuronal activity occurring in the brain. Status epilepticus (SE) is a single, continuous seizure lasting more than five minutes or two or more seizures within five minutes without regaining consciousness in between. It is a complication of epilepsy and medical emergency.

Answer 175

- ABCDE approach (Airway, Breathing, Circulation, Disability, Exposure) + high-flow oxygen - 1st line: 4mg IV Lorazepam, if ineffective then Lorazepam again then phenytoin

Answer 176

Spinal cord compression (SCC) is as a result of trauma to the spinal cord and can cause injury to the spinal cord due to external pressure. This damages the white and grey matter and causes loss of all or some of the sensory modalities and motor functions. Spinal cord compression/injury affects the spinal cord (above L1 - L2). For SCC affecting regions below L1 - 2, it is known as cauda enquina syndrome.

Answer 177

- Trauma: car accidents, falls - Vertebral compression fractures: osteoporosis, osteomalacia - Intervertebral disc disease: disc herniation - Tumours: metastatic disease, CNS tumours - Infection: osteomyelitis

Answer 178

Symptoms: 1) Acute onset: more likely trauma or disc herniation 2) Insidious onset: more likely malignancy, osteoporosis - Back pain - Paresthesia - Weakness - Bladder or bowel dysfunction Signs: 1) Upper motor neuron weakness below lesion (often presents after spinal shock): - Loss of muscle power - Increased tone - Hypereflexia 2) Sensory deficit: fine-touch, vibration, temperature, (affecting dorsal column medial lemniscus (fine-touch) and spinothalamic tracts (pain + temp, crude touch + pressure) 3) Spinal shock: - Hypo- or areflexia below the level of injury - Motor paralysis below the level of injury 4) Neurogenic shock: - Typically, cervical/high thoracic injury - Bradycardia - Peripheral vasodilation - Decreased cardiac output - Priapism (prolonged erection)

Answer 179

1) Complete spinal cord injury 2) Central cord syndrome (usually affects the cervical spine) 3) Anterior cord syndrome (disruption of anterior spinal cord/artery) 4) Posterior cord syndrome (Disruption of posterior spinal cord) 5) Brown-Sequard syndrome (Hemisection lesion of the spinal cord)

Answer 180

Loss of motor and sensory function below the SCI level E.g. high cervical cord level - quadriplegia, respiratory insufficiency, loss of bladder and bowel function, neurogenic shock

Answer 181

- Hemisection lesion of the spinal cord, results in: - Unilateral spastic paralysis - Ipsilateral loss of vibration and proprioception (DCML - decussate at medulla oblongata) - Contralateral loss of pain and temperature sensation (spinothalamic tract - decussates in spinal cord)

Answer 182

Primary investigations: - Full neurological examination: tone, power, sensation, reflexes, proprioception - MRI of whole spine: diagnostic, and shows affected area as compressed. But spinal cord injury without radiographic abnormality (SCIWRA) may occur (cannot detect on MRI)

Answer 183

Depends on the underlying cause and requires MDT input. 1) VTE prophylaxis: due to reduced mobility 2) Nutritional input: if dysphagia or reduced oral intake 3) Blood pressure support 4) Ventilatory support: if high cervical lesion affects respiratory effort 5) Physiotherapy

Answer 184

1) Immediate immobilisation 2) Definitive treatment: surgical spinal cord decompression and IV corticosteroids (not used in SCC caused by gunshots)

Answer 185

- Dexamethasone: reduce inflammation - Radiotherapy: usually performed as a palliative measure in metastatic disease - Surgery: depending on impact of radiotherapy, age and prognosis

Answer 186

- IV antibiotics - Surgery: spinal cord decompression vs CT-guided needle aspiration if antibiotic therapy is insufficient

Answer 187

Sciatica refers to the symptoms associated with irritation of the sciatic nerve.

Answer 188

The main causes of sciatica are lumbosacral nerve root compression by: 1) Herniated disc 2) Spondylolisthesis (anterior displacement of a vertebra out of line with the one below) 3) Spinal stenosis

Answer 189

The spinal nerves L4 – S3 come together to form the sciatic nerve. The sciatic nerve supplies sensation to the lateral lower leg and the foot. It supplies motor function to the posterior thigh, lower leg and foot. Sciatica causes unilateral pain from the buttock radiating down the back of the thigh to below the knee or feet.

Answer 190

- Unilateral “electric” or “shooting” pain from buttock > back of thigh > below knee or feet - Other symptoms: - Paraesthesia (pins and needles) - Numbness - Motor weakness Bilateral sciatica is a red flag for cauda equina syndrome.

Answer 191

- Sciatic stretch test - Patient lies on back, examiner lifts one leg to 80 - 90 degrees - Examiner dorsiflexes patient's ankle - Pain buttock/posterior thigh indicates sciatic nerve root irritation - Symptoms improve with flexing the knee.

Answer 192

Low risk of chronic back pain: - Self-management, education, reassurance - Analgesia (1st line is NSAIDS, then codeine, benzodapines (diazepam)) - Staying active and continuing to mobilise as tolerated Additional options for medium/high risk: - Physiotherapy - Group exercise - Cognitive behavioural therapy Specialist management options for chronic sciatica include: - Epidural corticosteroid injections - Local anaesthetic injections - Radiofrequency denervation - radiofrequency is used to target the nerves that supply sensation to the joints associated with back pain - Spinal decompression

Answer 193

A group of neurodegenerative disorders characterised by the selective loss of neurons in the motor cortex, cranial nerve nuclei and anterior horn cells. Motor neurone disease is a progressive, ultimately fatal condition where the motor neurons stop functioning. There is no effect on the sensory neurons and patients should not experience any sensory symptoms. Amyotrophic lateral sclerosis (ALS) is the most common (50% cases)

Answer 194

- A condition characterised by the loss of neurons in the motor cortex and anterior horn - UMN (mainly corticospinal tract affected) + LMN signs (anterior horn cells affected) - Babinski response - indicates UMN lesion, non-specific (toe dorsiflexion on plantar stimulation) - Upper extremity weakness (UMN/LMN) - Stiffness, with poor co-ordination and balance (LMN) - Spastic, unsteady gait (UMN weakness affecting lower limbs) - The familial form is associated with mutations in superoxide dismutase (SOD1)

Answer 195

LMN signs: predominantly affects the anterior horn cells Best prognosis

Answer 196

UMN signs: predominantly affects the corticospinal tracts - which transmit motor control of voluntary movements from the primary motor cortex to effector muscles.

Answer 197

Affects the suprabulbar nuclei and cranial nerves, producing speech and swallow issues - Dysphagia, chewing difficulties - Flaccid tongue - Speech is hoarse, quiet, nasal Worst prognosis

Answer 198

UMN carry motor impulses from the brain to the LMN. Neurotransmitter = glutamate

Answer 199

Hypertonia - everything goes up - Spasticity (combo of paralysis, increased deep tendon reflexes and hypertonia) - Clonus ( involuntary muscle contractions) - Increased reflexes (hyperreflexia) More detail: - Increased muscle tone→ Spasticity - Clasp-knife response: Initial higher resistance to movement is followed by a lesser resistance - Increase in deep tendon reflexes (e.g. biceps) and decrease in superficial reflexes (e.g. abdominal) - Flexors weaker than extensors in the legs - Extensors weaker than flexors in the arms - Babinski sign: Big toe raised rather than curled when the bottom of the foot is stimulated - Minimal atrophy and fasciculations

Answer 200

- Hypotonia - everything goes down - Muscle wasting (atrophy) - Reduced reflexes (hyporeflexia) - Fasciculations More detail: - Decreased muscle tone - Muscle paralysis - Weakness and wasting (atrophy) - Arreflexia (Absence of the relevant reflex) - Muscle fasciculation (twitching)- results from random and spontaneous depolarization of a motor neuron or axon

Answer 201

LMN carry motor impulses from the UMN to muscles Neurotransmitter = acetylecholine

Answer 202

- Advancing age = onset > 40 and average age 60 - Male gender: 1.2 to 1.8x more likely - Family history: familial in 5% of cases and the SOD1 mutation is implicated - Smoking: ‘probable’ risk factor

Answer 203

Clinical diagnosis, but investigations can be conducted to rule out other pathology Investigations to consider: - Electromyography: in MND there will be evidence of fibrillation potentials (irregular contractions) - Nerve conduction studies: may show modest reductions in amplitude - MRI spine: imaging can help exclude spinal pathology which may mimic MND, such as cervical cord compression and myelopathy - Pulmonary function tests: patients with MND are at risk of respiratory failure

Answer 204

1) Riluzole: ALS - prolongs survival by 2-4 months, thought to protect motor neurons from glutamate-induced damage 2) Respiratory support: patients with reduced FVC (forced vital capacity) can use non-invasive ventilation at home, usually BiPAP; prolongs survival by 7 months 3) Supportive treatment: - Antispasmodics: such as baclofen - Feeding and nutritional support: often with PEG tube (directly into stomach) - Speech and language therapy - Physiotherapy

Answer 205

Motor innervation to all extraocular muscles (SR, MR, IR, IO, LPS) apart from lateral rectus and superior oblique. Dysfunction = ptosis, down and out eye and fixed dilated pupil

Answer 206

Superior oblique of the eye (intorsion, depression and abduction) Dysfunction (caused by trauma) - diplopia (double vision) when looking down

Answer 207

Trigeminal - ophthalmic, maxillary and mandibular Ophthalmic - sensation to frontal, ethmoid and sphenoid sinuses Maxillary - sensation to maxillary and sphenoid sinuses Mandibular - sensation to anterior 2/3 tongue Motor to mastication muscles Lesion causes: - Jaw deviates towards the affected side - Loss of corneal reflex - Trigeminal neuralgia

Answer 208

Innervates lateral rectus - abduction of eye Ipsilateral loss of gaze abduction from midline Adducted eye - a sign of increased intracranial pressure

Answer 209

- Motor: Facial muscles - Sensory: taste to anterior 2/3 tongue Parasympathetic: - Lacrimal glands - Submandibular & sublingual salivary glands Lesions cause: - Facial drooping with NO forehead sparing - Bell's palsy (facial paralysis with temporary inability to control the facial muscles on the affected side) Treatment for Bell's palsy = oral prednisolone

Answer 210

Vestibules and cochlea, invovled in: - Hearing (cochlear branch) - Balance (vestibular branch) Lesions cause: - Hearing loss - Loss of balance - Caused by Paget's disease, compression or middle ear disease

Answer 211

CN IX: - Motor innervation to parts of the larynx - Taste and sensation to posterior third of tongue - Parasym to parotid glands CN X: - Sensory innervation to oesophagus, lungs, trachea, heart and most of digestive tract, parts of the pharynx - Motor innervation to larynx - Parasym to trachea smooth muscles, bronchi, GI tract and regulates heart rhythm Lesions will cause: - Impaired gag reflex - Swallowing, respiratory, GI and vocal difficulties, urinary retention - uvular deviation to the unaffected side - Caused by jugular foreman lesion

Answer 212

Innervates sternocleidomastoid (turn head side to side) & trapezius muscle (shrug shoulders) - so can't turn head or shrug shoulders.

Answer 213

Motor innervation of the tongue normally, so lesion causes the tongue to deviate to side of lesion.

Answer 214

Myasthenia gravis is a chronic autoimmune disorder of the postsynaptic membrane at the neuromuscular junction of skeletal muscle. It occurs due to circulating autoantibodies against the nicotinic acetylcholine receptor (AChR). Some patients also have antibodies against muscle-specific kinase (MuSK), a postsynaptic protein.

Answer 215

- Female - 2x more likely - Family history of autoimmune disease

Answer 216

Myasthenia Gravis occurs due to circulating autoantibodies against the nicotinic acetylcholine receptor (AChR). A small proportion of patients also have antibodies against muscle-specific kinase (MuSK), a postsynaptic protein. Ultimately, this causes fewer available binding sites for acetylcholine (Ach) at the postsynaptic membrane, resulting in muscle weakness.

Answer 217

Hallmark symptom - fatigability - muscles become progressively weaker during activity and improve upon rest. Extraocular muscles are first affected, presenting with diplopia. Symptoms - Lethargy - Muscle weakness gets worse at the end of the day - Double vision - Slurred speech - Dysphagia (swallowing difficulties) - Shortness of breath: may suggest a myasthenic crisis Signs: - Proximal muscle weakness with fatigability: often affecting the face and neck - Ptosis exacerbated on upward gaze: may be bilateral or unilateral - Myasthenic snarl: a ‘snarling’ expression when attempting to smile

Answer 218

Primary investigations: 1) Antibodies: AchR antibodies are 1st line, whilst anti-MuSK can also be tested in patients who are AchR antibody negative 2) Electrophysiological studies: repetitive nerve stimulation shows a decremental muscle response 3) CT thorax: to exclude a thymoma 4) Thyroid function tests: as there is a higher prevalence of autoimmune thyroiditis

Answer 219

- Repeated blinking will exacerbate ptosis - Prolonged upward gazing will exacerbate diplopia on further eye movement testing - Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides

Answer 220

1st line: acute treatment is prednisolone, long-term is pyridostigmine; an acetylcholinesterase inhibitor

Answer 221

A complication of myasthenia gravis due to the weakening of the respiratory muscles and is often provoked by infections or medications. Patients present with increasing SOB > respiratory failure

Answer 222

- IV immunoglobulin or plasmapheresis (plasma exchange) - Non-invasive ventilation with BiPAP (Bilevel positive airway pressure) - Intubation: if severe respiratory compromise - Corticosteroids may be used as adjuvant therapy

Answer 223

Cauda equina syndrome (CES) is a neurosurgical emergency which occurs when the bundle of nerves below the end of the spinal cord are compressed.

Answer 224

The cauda equina, which is Latin for ‘horse’s tail’, is a bundle of lumbar, sacral and coccygeal nerve roots (L1-S5). At around the vertebral level of L1, the spinal cord terminates as the conus medullaris, and the cauda equina begins. These nerves supply the pelvic organs and lower limbs: Sensation to the lower limbs, perineum, bladder and rectum Motor innervation to the lower limbs and the anal and urethral sphincters Parasympathetic innervation of the bladder and rectum

Answer 225

Lumbar disc herniation: the most common cause of CES Trauma Spinal tumour Lumbar spinal stenosis: narrowing of the spinal cord may result in CES. Some causes include spinal osteoarthritis (spondylosis) Epidural abscess or haematoma

Answer 226

Symptoms 1) Lower back pain and sciatica (97%) 2) RED FLAG Saddle anaesthesia’: numbness in the peri-anal region, groin and inner thighs (93%) - patients might describe this as ''numbness when wiping" 3) Bladder and bowel dysfunction: urinary retention and faecal incontinence 4) Lower limb weakness Signs 1) LMN signs (ipsilateral hypotonia, fasciculations and hyporeflexia) 2) Palpable bladder due to urinary retention

Answer 227

Primary investigations: MRI spine: gold-standard investigation and must be requested urgently - visualisation of lesion and compression of neural structures Bladder ultrasound: to determine whether urinary retention

Answer 228

Metastatic spinal cord compression (MSCC) - when a metastatic lesion compresses the spinal cord (before the end of the spinal cord and the start of the cauda equina). MSCC presents similarly to cauda equina, with back pain and motor and sensory signs and symptoms. A key feature is back pain that is worse on coughing or straining. MSCC is an oncological emergency and requires rapid imaging and management.

Answer 229

Emergency decompressive laminectomy (operation to remove vertebral bone (lamina): surgery should be performed within 24-48 hours of symptom onset All patients with suspected CES should be urgently referred to neurosurgery. Corticosteroids or radiotherapy: may be considered in certain patients with CES secondary to malignancy

Answer 230

1) Non-polarising neuromuscular blockade - muscle relaxant during surgery 2) Atracurium antagonizes the neurotransmitter action of acetylcholine by binding competitively with cholinergic receptor sites at the NMJ 3) Flushing; hypotension

Answer 231

1) Acute pain 2) It behaves as an agonist at a complex group of receptors (the μ (mu), κ (kappa) and δ (delta subtypes) that are normally acted upon by endorphins. 3) Arrhythmias; confusion; constipation; dizziness; drowsiness; eurphoria

Answer 232

1) Reversal of hypotension from spinal or epidural anaesthesia, reversible airway obstruction 2) Increases BP by stimulating heart rate, and cardiac output. Causes bronchodilation due to the activation of beta-adrenergic receptors in the lungs. 3) Anxiety; headache; insomnia; nausea

Answer 233

1) Pyrexia, mild to moderate pain 2) a weak inhibitor of prostaglandin synthesis, a molecule involved in pain and inflammation 3) Rare: thrombocytopenia, abnormal livre function

Answer 234

Excessive ingestion (toxic overdose is defined as ingestion of paracetamol >75mg/kg) leading to acute liver failure Normally, 90% conjugated to glucuronic acid in the liver > non-toxic compounds > excreted in urine A small proportion is converted by cytochrome P450 to toxic metabolite > detoxified by conjugation with glutathione. Glutathione depleted in overdose > hepatic necrosis

Answer 235

If ingestion less than 1 hour ago + dose >150mg/kg: Activated charcoal If staggered overdose or ingestion >15 hours ago: N-acetylcysteine If ingestion <4 hours ago: Wait until 4 hours to take a level and treat with N-acetylcysteine based on level If ingestion 4-15 hours ago: Take an immediate level and treat based on level

Answer 236

1) Anaesthesia as a skeletal muscle relaxant to facilitate tracheal intubation and mechanical ventilation 2) Neuromuscular blockade by mimicking acetylcholine at the NMJ, but hydrolysis is much slower, and depolarisation is prolonged 3) Arrhythmias; bradycardia (repeated doses); flushing

Answer 237

1) Opioid painkiller for moderate to severe pain 2) Inhibits the reuptake of the natural neurotransmitters noradrenaline and serotonin and also binds weakly to μ-opioid receptors, blocking pain signal transmission to the brain 3) Arrhythmias; confusion; constipation

Answer 238

Syncope refers to a transient loss of consciousness due to disruption of blood flow to the brain, often leading to a fall.

Answer 239

1) Neurally-mediated reflex syncope - - Vasovagal syncope, carotid sinus syncope and situational faint Parasympathetic hyperactivity and/or sympathetic hypoactivity → ↓CO 2) Orthostatic syncope - failure of compensatory mechanisms to maintain CO when standing up 3) Cardiac syncope: arrhythmias or structural defects leading to reduced CO

Answer 240

- Vasovagal - Emotional stress (primary) - Vasovagal - extended standing in a warm environment, such as a school assembly (primary) - Situational - Post-exercise (primary) - Carotid - carotid sinus massage

Answer 241

- Parkinson's disease because of meds (primary) - Dehydration (primary) - Diabetes because of dehydration due to frequent urination and damage to blood vessels (secondary)

Answer 242

- AV node block (arrhythmia) - Valvular heart disease (structural) - Ischaemic heart disease (structural)

Answer 243

Depends on cause: Lying and standing blood pressure: to look for underlying orthostatic hypotension fall in SBP ≥ 20 mmHg and/or DBP ≥ 10 mmHg within 3 minutes of standing ECG: assess for cardiogenic cause FBC: to check for anaemia Glucose: hypoglycaemia can present similarly B-hCG: assess for ectopic pregnancy in females presenting with syncope

Answer 244

Neurally-mediated syncope: - Avoid triggers in primary syncope. Management of underlying pathology: Cardiac syncope - AV node block - packmaker indicated for high-grade Orthostatic syncope - Medication review: anti-hypertensives, diuretics can cause orthostatic syncope - Hydration: ensure good fluid intake - Compression stocking: prevent venous pooling

Answer 245

Acute coronary syndrome, ventricular arrhythmia, AV node block

Answer 246

A condition that develops due to damage to extremities, e.g. hands, feet, and arms. Diabetes mellitus type 1 and 2 are the most common cause of peripheral neuropathy in the UK - known as diabetic neuropathy. Hyperglycaemia and hypertriglyceridemia contribute to the pathogenesis of neuropathy in T1 and T2 DM.

Answer 247

- Usually asymptomatic but can present with: - Pain (peripheral) - Loss of sensation (peripheral) - Dysaesthesia (peripheral) - (abnormal sensation of burning, tingling, and numbness due to peripheral nerve lesion) - Reduced or absent ankle reflexes (peripheral) - Painless injuries (peripheral)

Answer 248

- Clinical diagnosis, but other routine tests can help rule out other causes - Fasting blood glucose - ≥ 7mmol/L - patients with peripheral neuropathy might not know they have DM - HbA1c > 6.5%/48mmol/mol - correlates with the level of glycaemic control

Answer 249

Without pain: - Glycaemic control through diet, exercise and medication (e.g. insulin injections) can help relieve neuropathic symptoms With pain - Glycaemic control as above and gabapentin as 1st line for painful DN

Answer 250

- Uraemia - Vitamin B12 deficiency - Hypothyroidism

Answer 251

Carpal tunnel syndrome is caused by compression of the medial nerve as it travels through the carpal tunnel in the wrist, causing pain and numbness in the median nerve distribution on the hand.

Answer 252

The flexor retinaculum is a fibrous band that wraps across the palmar side of the wrist. Carpal tunnel runs through between carpal bones and the flexor retinaculum. It contains: - Median nerve - Forearm flexor tendons The palmar digital cutaneous branch of the median nerve which runs through the carpal tunnel, supplies sensory innervation of the palms and thumb, index, middle and lateral half of ring finger The median nerve = motor supply for the three thenar muscles = thumb movement - Abductor pollicis brevis (thumb abduction) - Opponens pollicis (thumb opposition – reaching across the palm to touch the tips of the fingers) - Flexor pollicis brevis (thumb flexion) Therefore, the above sensory and motor innervations are affected in carpal tunnel syndrome aka compression of contents of the carpal tunnel

Answer 253

Sensory symptoms in the areas supplied by palmar digital cutaneous branch of the median nerve - palms, thumb, index, middle and lateral half of ring finger: - Numbness - Paraesthesia (pins and needles or tingling) - Burning sensation - Pain Worse at night, wake patient up, shake hands to relieve symptoms Motor symptoms of carpal tunnel syndrome affect the thenar muscles, with: - Weakness of thumb movements - Weakness grip - Difficulty with fine movements involving the thumb - Thenar muscle atrophy

Answer 254

- Phalen’s test - ask patient to flex wrist by putting back of two hands together - triggers sensory symptoms including numbness and paraesthesia - Tinel’s test - doctors tap patient's wrist where the median nerve travels through the carpal tunnel - numbness and paraesthesia in the median nerve distribution - Electromyogram - gold standard test to see how well small electrical currents travel through median nerve

Answer 255

Mild Conservative - rest and altered activity 1st line: wrist splints (neutral or 20° extension) worn every night for 1 month. Moderate/severe 1st line: surgical release - Open (with a vertical incision at the wrist) or endoscopic (keyhole) surgery. The flexor retinaculum (AKA transverse carpal ligament) is cut to release the pressure on the median nerve.

Answer 256

- Osteoarthritis (OA) - Stroke, acute

Answer 257

Difficulties with foot dorsiflexion due to peroneal neuropathy. The common peroneal nerve It supplies the tibialis anterior muscle (via its branch the deep peroneal nerve). This muscle dorsiflexes the ankle and therefore damage to its innervation leads to foot drop. Most often caused by: - Sports injuries - Herniated spinal disc - Peripheral neuropathy caused by diabetes - Hip or knee replacement surgery

Answer 258

An unpleasant sensory and emotional experience associated with actual or potential tissue damage.

Answer 259

- Acute pain – new onset of pain - Chronic pain – pain present ≥ 3 months

Answer 260

Pain is subjective - Sensory – the sensory signal transmitted from the nociceptors (pain receptor) (“it is a sharp sensation, likely a needle”) - Affective – the unpleasant emotional reaction to the pain (“it is excruciating, I can’t bear it”)

Answer 261

Pain receptors (nociceptors) at the ends of nerves detect damage/potential damage to tissues. Nerve signals transmitted along the afferent sensory nerves to the spinal cord (primary afferent nociceptors). Part of PNS. Two groups of nerve fibres transmit pain: - C fibres (unmyelinated and small diameter) – transmit signals slowly and produce dull and diffuse pain sensations - A-delta fibres (myelinated and larger diameter) – transmit signals fast and produce sharp and localised pain sensations Signal travels to CNS through the spinal cord using the spinothalamic tract to the brain where it is interpreted as pain, mainly in the thalamus and cortex.

Answer 262

There are three steps to the analgesic ladder: treat with lower steps before moving up if ineffective. Step 1: Non-opioid medications such as paracetamol and NSAIDs Step 2: Weak opioids such as codeine and tramadol (an SNRI and agonist of opioid receptors) Step 3: Strong opioids such as morphine, oxycodone, fentanyl and buprenorphine Other meds that can be combined with the above or used to treat neuropathic pain - Amitriptyline – a tricyclic antidepressant - Gabapentin – an anticonvulsant - Capsaicin cream (topical) – from chilli peppers

Answer 263

Abnormal growths within the brain. They vary from benign tumours (e.g. meningiomas) to highly malignant (e.g. glioblastomas). Often asymptomatic when small and present with focal neurological symptoms and symptoms of raised ICP as they increase in size.

Answer 264

Gliomas are tumours of the glial cells in the brain or spinal cord. There are three types from most to least malignant: - Astrocytoma - glioblastoma multiforme is the most common (95%) - Oligodendroglioma < 5% - Ependymoma

Answer 265

Tumours growing from the cells of the meninges in the brain and spinal cord. They are usually benign, however they take up space and this mass effect can lead to raised intracranial pressure and neurological symptoms.

Answer 266

Benign tumours arising from the pituitary glands. Can press on optic chiasm to cause bitemporal hemianopia. They can also cause hormone deficiencies (hypopituitarism) or to release excessive hormones leading to: - Acromegaly - Hyperprolactinaemia - Cushing’s disease - Thyrotoxicosis

Answer 267

- Lung (NSCC). - Breast. - Malignant melanoma. - Kidney.

Answer 268

1. Raised ICP. 2. Progressive neurological deficit. 3. Epilepsy

Answer 269

1. Headache. 2. Drowsiness. 3. +/- vomiting.

Answer 270

1. Worst first thing in the morning. 2. Worst when coughing, straining or bending forward.

Answer 271

Papilloedema - optic disc swelling Due to raised intracranial pressure caused by obstruction of venous return from the retina.

Answer 272

- Altered mental state - Visual field defects - Seizures (particularly focal) - Unilateral ptosis - Third and sixth nerve palsies

Answer 273

Grade 1: astrocytoma - these are often removed with surgery and may not need further treatment. Grade 2 astrocytoma, or a low-grade diffuse astrocytoma (may transform into high-grade tumour) Grade 3: ‘anaplastic astrocytoma’ - cancer. Grade 4: glioblastoma multiforme (GBM).

Answer 274

Concerning features of a headache that should prompt further examination and investigation include: - Constant - Nocturnal - Worse on waking - Worse on coughing, straining or bending forward - Vomiting

Answer 275

- MRI head - diagnostic - Visual field testing - visual field defect may be present - CT head - used to rule out other causes of symptoms e.g. herniation, stroke, haemorrhage or when MRI unavailable

Answer 276

Initial management is dexamethasone and mannitol for cerebral oedema Then: - Resective surgery. - Adjuvant chemotherapy with Temozolomide. - Palliative care.

Answer 277

- Surgery and adjuvant radiotherapy. - Chemotherapy. - Supportive care.

Answer 278

- Trans-sphenoidal surgery - Radiotherapy - Bromocriptine to block prolactin-secreting tumours - Somatostatin analogues (e.g. octreotide) to block growth hormone-secreting tumours

Answer 279

- Brain metastasis (secondary brain tumour) - Brain abscess - Multiple sclerosis

Answer 280

1) Epilepsy, generalized seizures, partial seizures 2) sodium channel blocker - block voltage-gated Na+ channels; inhibition of action potentials in excitatory neurons; ↓ seizure activity 3) Gastrointestinal problems, thrombocytopenia, leukopenia, DRESS (allergic reaction - Drug reaction with eosinophilia and systemic symptoms) 4) Tetrageneic

Answer 281

1) Epilepsy, generalized seizures, partial seizures - not suitable for people with AV block and Hx of bone marrow depression 2) sodium channel blocker - block voltage-gated Na+ channels; inhibition of action potentials in excitatory neurons; ↓ seizure activity 3) Pancreatitis, hepatotoxicity, renal dysfunction, AV block Boxed warning: SJS (Steven-Johnson syndrome), bone marrow depression

Answer 282

- Intracerebral haemorrhage - TIA - Hypoglycaemia

Answer 283

- Ischaemic stroke - Hypoglycaemia

Answer 284

- Epidural haematoma - "lucid" interval, associated with skull fracture - Intracerebral haematoma - Stroke

Answer 285

Aortic dissection

Answer 286

- Encephalitis - Viral meningitis - Drug-induced meningitis DDx for viral meningitis is bacterial meningitis and the other two above

Answer 287

A seizure that involves brief changes in awareness - typically involves behavioural arrest or staring lasting 5 to 10 seconds

Answer 288

Acoustic neuromas are tumours of the Schwann cells surrounding the auditory nerve that innervates the inner ear. They are slow-growing but eventually grow large enough to produce symptoms and become dangerous. Acoustic neuromas are usually unilateral. Bilateral acoustic neuromas are associated with neurofibromatosis type 2. Classic symptoms of an acoustic neuroma are: Hearing loss Tinnitus Balance problems They can also be associated with a facial nerve palsy.

Answer 289

Acoustic neuroma, classically presenting with unilateral deafness and vertigo occurring later, in addition to left-sided lesions of cranial nerves V, IX and X