Neurology Flashcards

Question

What are the causes of haemorrhage stroke?

Answer 1

* Brain bleeds: trauma, aneurysm rupture causing subarachnoid haemorrhage, anticoagulation, thrombolysis, carotid artery dissection * Atherothromboembolism * Vasculitis.

Answer 2

Increased blood pressure, smoking, diabetes mellitus, heart disease (vascular, ischaemic, AF), peripheral vascular disease, age, smoking, drinking alcohol, increased lipids, obesity, increased clotting (increased plasma fibrinogen and decreased antithrombin), combined pill, increased homocysteine, increased packed cell volume, carotid bruit, syphilis, past TIA, ethnicity (black or Asian).

Answer 3

Usually atherosclerotic plaque or clot in large artery ruptures, travels downstream, and gets trapped in narrower artery of the brain. Ischaemia -> infarction -> death of neural tissue -> loss of functionality. Embolic strokes are common complications of AF and atherosclerosis of carotids.

Answer 4

Bleeding from a single vessel within the brain, high blood pressure being the main cause.

Answer 5

Anterior circulation infarcts (middle cerebral artery, anterior cerebral artery, internal carotid, ophthalmic arteries): • MCA infarction: contralateral hemiplegia (muscle weakness/paralysis) on one side of the body, facial weakness, contralateral sensory loss, dysphagia (speech problems only if stroke is in dominant hemisphere, Broca’s), aphasia (inability to understand is Wernicke’s or produce speech is Broca’s, in dominant hemisphere stroke), facial droop, eye deviation towards the affected eye • ICA infarction: similar to MCA but collateral circulation may reduce the infarct size • ACA infarction: less common than MCA, hemiparesis affecting the leg more than the arm (contralateral weakness and sensory loss of the lower limb) truncal ataxia, incontinence, drowsiness, logical thinking, personality, frontal lobe deficits e.g. apathy or apraxia. • Cerebral hemisphere infarcts: most commonly occlusion of branch of MCA, with collateral circulation protecting the cortex, leading to infarction of the internal capsule (deep structures). Posterior circulation infarcts: • PCA infarction: contralateral hemianopia from unilateral lesions, cortical blindness from bilateral lesions (Anton’s syndrome), confusion or memory impairment because the PCA supplies the thalamus and posteromedial temporal lobe • Posterior circulation (vertebrobasilar artery): more catastrophic due to wide region supplied. Disorders of balance and coordination • Basilar artery thrombosis: high lesions cause midbrain infarction including coma and locked-in syndrome. • Cerebellar infarcts • Brainstem infarcts: includes basilar artery thrombosis. Also lateral medullary syndrome (Wallenberg’s syndrome) which is caused by occlusion of posterior inferior cerebellar artery. Presents with sudden vomiting and vertigo, Horner’s syndrome, ipsilateral facial numbness, dysarthria, limb ataxia, dysphagia and contralateral loss of pain and temperature • Lacunar infarcts (basal ganglia, internal capsule, thalamus and pons): often symptomless. Haemorrhage: headaches, altered mental status, seizures, nausea and vomiting. Watershed/border zone infarctions: causes by severe cerebral hypoperfusion such as hypotension after cardiac arrest. Ischaemia in the border zones between areas supplied by the ACA, MCA and PCA. Affects the parieto-occipito cortex, hippocampi and motor pathways. Complex patterns of visual loss e.g. Balint’s syndrome, memory loss, intellectual impairment, motor deficits and a vegetative state in prolonged cerebral hypoperfusion.

Answer 6

* Slurred speech * Arm/leg weakness * Facial drooping.

Answer 7

Immediate (within 1 hour): • CT scan • Bloods: FBC (look for thrombocytopenia and polycythaemia), blood glucose (rule out hypoglycaemia), clotting studies if anticoagulated. Further (within 24 hours): • Bloods: FBC, ESR, glucose, lipids, clotting studies • ECG and later 24 hour ECG: look for AF and cardioembolic stroke • Carotid Doppler studies: in patients with anterior circulation stroke. Others: • CT or MR angiography for carotid artery stenosis • MRI brain scan with dissection protocol • Cardiac monitoring • Vasculitis screen: increased ESR, ANCA, VDRL test for syphilis • Antiphospholipid antibodies (antiphospholipid syndrome is prothrombotic) • Thrombophilia screen • Genetics for CADASIL and mitochondrial disorders • Alpha-galactosidase for Fabry’s disease • Drugs of abuse screen e.g. cocaine • Chest X-ray to look for cardiomegaly (enlarged left atrium) • Hypertension: look for retinopathy, nephropathy or cardiomegaly • Look for hypoglycaemia, hyperglycaemia, dyslipidaemia, hyperhomocysteinaemia • Check for hyperviscosity: e.g. polycythaemia, sickle-cell disease • Check for thrombocytopenia and other bleeding disorders.

Answer 8

Low risk: • Refer for specialist assessment within 7 days of the onset of symptoms • Start aspirin immediately and them move to clopidogrel or continue current standard dose if already on an antiplatelet (unless on an anticoagulant) • Start an anticoagulant if cardiac source of emboli • Statin • ACE-i/ARB for blood pressure • No driving until seen by a specialist. High risk: • Assessment within 24 hours • As above. Modify risk factors e.g. stop smoking, less alcohol, exercise, diet, BP (aim for <145/85), hyperlipidaemia, diabetes mellitus. Surgery: carotid endarterectomy to remove build-up of fatty deposits (plaque). If tolerated, preferred to angioplasty with stenting as less chance of stroke from procedure. 1. Immediate general medical measures: airway, oxygen by mask, monitor blood pressure 2. Determine if thromboprophylaxis is appropriate: if so, immediate brain imaging 3. Brain imaging: CT to exclude haemorrhage and will show other pathology and sometimes infarction (<1 hour). MRI is best for acute infarct 4. If CT excludes haemorrhage, give immediate thrombolytic therapy (should be <4.5 hours after onset of symptoms), alteplase therapy. CI if stroke or head injury in last 3 months, history of intracranial haemorrhage, GI bleed in the last 21 days, major surgery in the last 14 days. IV alteplase is a tissue plasminogen activator. If CI, give aspirin. If CT confirms haemorrhage, give no drugs that could interfere with clotting. 5. Admit to MDT stroke unit: assess swallowing, start thromboembolism prophylaxis.

Answer 9

A recurrent throbbing headache often preceded by an aura and associated with nausea, vomiting and visual changes.

Answer 10

In females in reproductive years, suggesting hormones have an influence.

Answer 11

May affect the patient’s eyesight with visual phenomena such as fortification spectra (zig-zag lines), shimmering or scotomas (black holes in visual field) but may also result in pins and needles, dysphagia and rarely weakness of limbs and motor function.

Answer 12

Unilateral motor or sensory symptoms resembling a stroke.

Answer 13

``` Remember CHOCOLATE: • C hocolate • H angovers • O rgasms • C heese • O ral contraceptives • L ie-ins • A lcohol • T umult (loud noise) • E xercise. ```

Answer 14

Changes in the arterial brainstem blood flow which causes unstable trigeminal nerve nuclei in the basal thalamus and causes release of vasoactive neuropeptides (CGRP and substance P). Leads to neurogenic inflammation, vasodilation and plasma protein extravasation. In aura, the cortical spreading depression is a self propagating wave of neuronal and glial depolarisation that spreads across the cortex.

Answer 15

``` A. 5 attacks fulfilling B-D B. Attacks last 4-72 hours C. Two of the following: Unilateral Pulsing Moderate/severe Aggravated by routine physical exercise D. During headache at least one of: Nausea and/or vomiting Photophobia (light sensitive) and phonophobia (sound sensitive). These are often premenstrual. ```

Answer 16

A. At least 2 attacks fulfilling B and C B. One or more reversible aura symptom: Visual: zigzags, spots Unilateral sensory: tingling numbness Motor weakness: known as ‘hemiplegic migraine’ so rule out stroke and TIA C. Two or more of the following 4: One or more aura symptoms spread gradually over 5 minutes and/or two or more aura symptoms occurring in succession Each aura symptom lasts 5-60 minutes One or more aura symptom is unilateral Aura accompanies/followed within 60 minutes by headache.

Answer 17

Prodrome occurs a while before the migraine and is a weird feeling of: yawning, cravings, mood/sleep changes.

Answer 18

Mainly based on clinical diagnosis. Neuroimaging. Examine: • Eyes for papilloedema and other eye issues • Blood pressure • Head and neck. Exclude other causes (including mass lesions): • Lab tests for CRP and ESR Neuroimaging indications red flags: • Worst/severe thunderclap headache: subarachnoid haemorrhage • Change in pattern of migraine • Abnormal neurological exam • Onset over 50 years • Epilepsy • Posteriorly located headache. Lumbar puncture indications: • Worst headache of life, thunderclap: subarachnoid haemorrhage • Severe rapid onset headache, progressive headaches, unresponsible headaches.

Answer 19

* Tension headache (bilateral, tight band around head) * Cluster headache * Medication over-use headache * Meningitis (fever, photophobia, stiff neck, purpuric rash, coma) * Subarachnoid haemorrhage (‘worst headache ever’, often occipital. neck stiff, focal signs, decreased consciousness) * Tumour * Cervical spondylosis * TIAs may mimic migraine aura * Encephalitis (fever, odd behaviour, fits or reduced consciousness).

Answer 20

Conservative: avoid triggers and ensure analgesic rebound headache s not a problem. Acute attacks: • Mild: NSAID/paracetamol +/- anti-emetic • Severe: oral triptan e.g. sumatriptan or nasal in 12-17 year olds. Non-pharmalogical: warm or cold packs to the head, or rebreathing into paper bag (increase PaCO2) may help abort attacks. Butterbur extracts or riboflaxin supplementation. Transcutaneous nerve stimulation may help.

Answer 21

1. Propranolol (beta-blocker) or Topiramate (anti-convulsant) 2. Acupuncture (10 sessions over 5-8 weeks) 3. Amitriptyline (tricyclic anti-depressant) 4. Botulinum toxin type A (only if not responded to at least 3 prior pharnalogical therapies and whose condition is appropriately managed for medication overdose).

Answer 22

Migraine often improves in pregnancy but if not they are associated with greater risk of pre-eclampsia and cardiovascular complications. First line is paracetamol. Triptans and NSAIDs can be used but discuss risks. Don’t use aspirin if breastfeeding . Anti-emetic: cyclizine or promethazine.

Answer 23

Incidence of migraine usually with aura and ischaemic stroke is increased by use of combined oral contraceptive pill.

Answer 24

If uncontrolled with standard treatment and predictable, consider use of frovatriptan or zolmitriptan on the days migraine is expected.

Answer 25

Can be episodic (<15 days per month) or chronic (>15 days per month for at least 3 months).

Answer 26

``` Primary (syndromes based on symptoms): • Migraine • Cluster • Tension. Secondary (associated with something else): • Meningitis • Subarachnoid haemorrhage • Giant cell arteritis • Idiopathic intracranial hypertension • Medication overuse headache. Other: • Trigeminal Neuralgia (facial pain). ```

Answer 27

``` Neurovascular irritation which refers to scalp muscles and soft tissues. Remember MC SCOLD: • Missed meals • Conflict • Stress • Clenched jaw • Overexertion • Lack of sleep • Depression. ```

Answer 28

A. 10 or more attacks occurring less than 1 day per month (less than 12 days per year) and fulfilling B-D B. Headache lasting 30 minutes to 7 days C. Headache has two of the following: Bilateral Pressing/tightening (non-pulsatile) quality Mild or moderate intensity/pain Not aggravated by routine physical activity (e.g. walking or climbing stairs) D. Both of the following: No nausea or vomiting (anorexia may occur) No more than one of photophobia and phonophobia E. Not attributed to another disorder.

Answer 29

* Reassurance and lifestyle advice * Stress relief by massage or acupuncture * Avoidance of cause * Medication e.g. paracetamol, NSAIDs (ibuprofen, diclofenac) or aspirin * Tricyclic anti-depressants e.g. amitriptyline * Avoid opioids * Limit analgesics to no more than 6 days per month to reduce risk of medication overuse headaches.

Answer 30

Cluster headaches.

Answer 31

Episodic: 2 or more cluster periods lasting 7 days to 1 year (usually 2-3 weeks) separated by pain free periods lasting one or more months. Chronic: attack occurring for one or more years without remission or with remission lasting less than one month.

Answer 32

``` Remember CHOCOLATE: • C hocolate • H angovers • O rgasms • C heese • O ral contraceptives • L ie-ins • A lcohol • T umult (loud noise) • E xercise. ```

Answer 33

A. At least 5 headache attacks fulfilling B-D B. Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 minutes if untreated and rises to crescendo C. Headache is accompanied by ipsilateral cranial autonomic features and/or sense of restlessness or agitation D. Attacks have a frequency from 1 every other day to 8 per day.

Answer 34

Rapid onset of excruciating pain around one eye that may become watery and bloodshot. Deemed to have a boring/hot poker characteristic. Associated with ipsilateral eye lacrimation and redness, facial flushing, rhinorrhoea (blocked nose), miosis (excessive pupil constriction) and/or ptosis (drooping or falling of upper eyelid). Usually occur in the middle of the night or morning hours. Occurs once or twice a day, usually at the same time. Pain raises to a crescendo over a few minutes and lasts for 15-180 minutes (average 30-100).

Answer 35

Acute attacks: SC sumatriptan, IM Zolmitriptan, 100% oxygen therapy (unless they have COPD).

Answer 36

First line: verapamil (calcium channel blocker), lithium, corticosteroids.

Answer 37

Chronic, debilitating condition resulting in intense and extreme episodes of pain. Knife like pain.

Answer 38

* Peak incidence between 50-60 * Female>male * Prevalence increases with age * May be due to genetic disposition.

Answer 39

• Vein or artery compressing the trigeminal nerve • Local pathology pressing on trigeminal nerve (more common in younger people) e.g. aneurysms, meningeal inflammation, tumours (e.g. vestibular schwannoma) • 5th nerve lesion: Brain stem: tumour, MS, infarction Cerebellopontine angle: acoustic neuroma, other tumour Petrous bone: spreading middle ear infection Cavernous sinus: internal carotid aneurysm, tumour, thrombosis of cavernous sinus.

Answer 40

The trigeminal nerve (CNS) has both motor and sensory functions and enters the brain at the level of the Pons. It has three divisions: ophthalmic, maxillary and mandibular. Compression of the trigeminal nerve results in demyelination and excitation resulting in erratic pain signalling.

Answer 41

A. At least 3 attacks of unilateral facial pain fulfilling B and D B. Occurring in one or more distributions of the trigeminal nerve, with no radiation beyond the trigeminal distribution C. Pain has at least 3 of the following: Reoccurring in paroxysmal attacks from 1 second to 2 minutes Severe intensity Electric shock like, shooting, stabbing or sharp Precipitated by innocuous stimuli to the affected side of the face D. No clinically evident neurological deficit. Paroxysms of intense, stabbing pain, lasting seconds in the trigeminal nerve distribution.

Answer 42

Exclude secondary causes or other pathologies.

Answer 43

First line: carbamezapine (anti-convulsant) Second line: Iamtrigine, phenytoin, gabapentin (analgesic targeted for neuropathic pain). Surgical (may be directed at the peripheral nerve, trigeminal ganglion or nerve root): • Microvascular decompression: relieves pressure on the nerve by separating blood vessels touching the nerve or wrapped around it • Stereotactic radiotherapy: concentrated beam of radiotherapy to deliberately damage the trigeminal nerve where it enters the brainstem. Length of pain and time to treat are limiting factors.

Answer 44

Intracranial pressure >15mmHg. Untreated raised ICP can lead to permanent sight loss, neurological deficit and death.

Answer 45

As volume of lesion increases, initially there isn’t a rise in ICP. This is because there is a compensatory reduction in CS. Will be able to see tight ventricles. This can only go so far and so the pressure begins to rise. There is an exponential rise in pressure: • Initially there is a given increase in pressure for a given increase in volume • As pressure increases, there is a greater increase in pressure for the same amount of volume. As lesion begins to expand, it pushes on adjacent structures. Begin to get pressure gradients across areas of division across the skull which causes displacement of tissue (foramen magnum and tentorium cerebelli). Sometimes, the outflow tract to ventricle is blocked and so there is paradoxical expansion of the ventricle.

Answer 46

Ipsilateral pupillary dysfunction dilatation is indicator of raised ICP. Occulomotor nerve compression causes an eye that is deviated down and out. Also carries parasympathetic innervation to pupil which arises from Edinger Westphal nucleus ad those parasympathetic travel along the oculomotor nerve whereas sympathetic fibres come from sympathetic chain coming up from the vessels. This gives unbalanced sympathetic tone so lose parasympathetic tone and pupil dilation. Compression of the PCA. The PCA supplies occipital lobe so may get secondary infarction of occipital lobe.

Answer 47

Headache, nausea and vomiting.

Answer 48

* Worse on waking (CSF redistribution when lying flat increases pressure around brain) * Worse when coughing, sneezing, straining * Postural: worse when lying down * Papilloedema: may be present if acute * Pupillary changes * +/- focal signs.

Answer 49

• Head CT • Ophthalmology review. Not a lumbar puncture as there is a risk of coning, at least until after imaging.

Answer 50

IV Mannitol. Surgical: shunt, decompression. Dexamethasone.

Answer 51

Headache present on 15 or more days per month.

Answer 52

Regular use for more than 3 months of one or more symptomatic treatment drugs: • Ergotamine, triptans, opioids or combination analgesic (paracetamol + codeine/opioid) medications on 10 or more days per month or for more than 3 months • Simple analgesics or any combination of ergotamine, triptans, analgesic opioids on 15 or more days per month or more than 3 months on a regular basis without overdose of any single class alone.

Answer 53

Analgesia must be withdrawn. Aspirin or naproxen for the rebound headache. Limit over the counter analgesic drug use to no more than 6 days per month.

Answer 54

Inflammation of the brain parenchyma. Confusion due to direct inflammation of the brain. Consider whenever odd behaviour and decreased consciousness is accompanied with an infectious prodrome (high temperature, rash).

Answer 55

Infections more frequent in children and elderly.

Answer 56

``` Usually viral: • Herpes simplex (by far the most common) • Varicella zoster (chicken pox) • Measles • Mumps • Rubella • EBV • HIV • CMV • Coxsackie. Other causes: • TB • Malaria • Japanese encephalitis virus • Tick-borne encephalitis • Rabies • West nile • Lyme disease • toxoplasmosis. Non-infective: • Autoimmune • Paraneoplastic. ```

Answer 57

Affects mainly the frontal and temporal lobes resulting in decreased consciousness, confusion and focal signs.

Answer 58

``` Hours to days before presentation: • Preceding “flu-like” illness. Then triad of: • Altered GCS: confusion, drowsiness and coma • Fever • Headache. Also, less commonly: • Seizures • Memory loss • Hemiparesis • Dysphagia • +/- history of meningism (stiff neck, vomiting and headache) if it has progressed to encephalitis from meningitis. Symptoms of raised ICP (vertigo, nausea, severe headache and photophobia). ```

Answer 59

MRI head: to show swelling/inflammation +/- midline shifting due to raised ICP. Often bilateral but can be asymmetrical. EEG: shows periodic sharp and slow waves. Lumbar puncture (after imaging): raised lymphocytic CSF, take CSF for viral PCR HIV test: acute phase viraemia can cause encephalitis. Bloods: FBC, U&Es, LFTs, TFTs, B12, lactate. Blood cultures and gram stain. CT to check for space occupying lesions.

Answer 60

Midline shift. Often bilateral but can be asymmetrical.

Answer 61

Mostly supportive. IV Aciclovir if suspected HSV or VZV. If seizures, give Carbamazepine. If meningitis is suspected, give IM benzyl penicillin. Be careful with fluids as could cause a cerebral oedema. Sedatives may be needed.

Answer 62

Shingles is a painful rash caused be the reactivation of a nerve infection caused by the varicella-zoster virus. Less infectious than the first infection.

Answer 63

Initial infection of Herpes Zoster (varicella-zoster) causes chicken pox. Reactivation causes shingles.

Answer 64

Old age, immunocompromised, chicken pox in <18 months age, HIV, malignancy.

Answer 65

Viral infection affecting the peripheral nerves. First presents in childhood as chicken pox and then Varicella lies dormant in the dorsal root ganglion. When reactivated, it travels down the affected peripheral nerve via the sensory root in dermatomal distribution over 3-4 days and this causes perineural and intramural inflammation.

Answer 66

* Pre-eruptive: no skin lesions but burning itching in one dermatome, usually a day or two before eruption * Dermatomal distribution of red, painful rash and pain (most commonly cervical, trigeminal, thoracis and lumbar dermatomes). Rash does not cross dermatomes * Malaise, myalgia, headache and fever * Itching * Fluid filled blisters * Stabbing/burning pain.

Answer 67

Rash that consists of papules and vesicles restricted to the same dermatome: • Neuritic pain • Crust formation and drying occurs over next week with resolution in 2-3 weeks • Rash does not extend outside dermatome.

Answer 68

``` Often a clinical diagnosis. Other: • PCR test • CSF analysis • Bloods and cultures. ```

Answer 69

Oral Aciclovir, valacyclovir, famiciclovir (antiviral therapy). If immunosuppressed, treat with IV acyclovir. Analgesia. Antipyretics.

Answer 70

Inflammation of the meninges.

Answer 71

Herpes simplex.

Answer 72

Inflammation of the meninges.

Answer 73

Bacterial.

Answer 74

Strep pneumoniae.

Answer 75

Gram positive diplococci.

Answer 76

Strep. Agalactaie and E.coli.

Answer 77

Listeria monocytogene.

Answer 78

Neisseria meningitis.

Answer 79

Non-blanching purpuric rash, necrosis, high mortality.

Answer 80

``` Bacteria (more serious)l: • Strep pneumoniae: most common in adults, gram positive diplococci • Neisseria meningitis: gram negative diplococci. 5-11% adult carriage, 25% in teenagers. If in blood culture think meningococcal septicaemia (non-blanching purpuric rash, necrosis, high mortality). • Strep. Agalactaie and E.coli: neonates • Listeria monocytogene: pregnant and older women, associated with immunosuppression • Group B strep: carried by up to 30% of pregnant women • Haemophilus influenzae B: children • Leptospira • Rickettsia • TB (presents with chronic) • Syphilis (presents with chronic) Viral (more common): • Coxsackie virus • Herpes simplex virus (HSV) • Varicella Zoster virus (VZV) • Enterovirus • HIV • Mumps • Echovirus • Cytomegalovirus (CMV) • EBV • Polio (very rare). Fungal: • Mainly in the immunosuppressed • Cryptococcal presents with chronic Parasitic: • P.Falciparum. Non-infective (occur with chronic presentation): • Paraneoplastic: cancer can cause inflammation which presents similarly • Drug side effects • Autoimmune e.g. vasculitis/SLE ```

Answer 81

Organisms seen on gram film.

Answer 82

No organisms seen.

Answer 83

Organisms seen on Phenol auramine/Ziehl Neelson stain.

Answer 84

Organisms seen on India ink stain.

Answer 85

HIV, immunocompromised.

Answer 86

Students, travel and immunosuppressed.

Answer 87

Polymorphs (neutrophils).

Answer 88

Lymphocytes.

Answer 89

Fibrin web.

Answer 90

Fibrin web.

Answer 91

Bacterial: low. Viral: normal. TB: low. Cryptococcal: low.

Answer 92

High opening pressure.

Answer 93

The brain and the CSF should be sterile and contain no bacteria. Bacteria can get in through different routes: • Neurosurgical complications: post-op, infected shunts, trauma • Extracranial infection: ear (otitis media), nasopharynx, sinuses (sinusitis) • Via the blood stream: e.g. bacteraemic seeding. Once the CSF is infected, the pathogen can multiply and replicate because there are no immune cells because the blood-brain barrier prevents movement from the blood. Eventually the white blood cells enter into the CSF, meninges and brain due to the blood vessels becoming leaky and this causes meningeal inflammation +/- brain swelling.

Answer 94

* Fever * Headache * Neck stiffness: “meningism”. May not be able to touch chin to neck. * Purpuric rash: only in bacterial. A non-blanching plupurent rash (petechiae) is meningococcal septicaemia * Photophobia and/or phonophobia * Papilloedema: swelling of the optic disc on fundoscopy. Usually bilateral * Nausea and vomiting * Irritability * Progressive drowsiness.

Answer 95

A non-blanching plupurent rash (petechiae).

Answer 96

* Kernig’s sign: when the patient is lying with hip flexed at 90 degreed, knee cannot be fully extended without causing back pain * Brudinski’s sign: passive flexion of the neck causes flexion of both legs and thighs * Glass test: blanching or non-blanching pupuric rash.

Answer 97

``` Lumbar puncture is diagnostic. It is done after GCS, blood cultures, broad spectrum antibiotics and steroids. Looks for: • Microscopy • Gram stain • Culture • Protein (raised) • Glucose (less than 2/3) blood • Viral PCR • Consider Acid Fast Bacilli (TB) and histology (for tumours). ```

Answer 98

* Abnormal clotting (platelets/coagulation) * Petechial/purpura rash: because suggests bloodborne virus so could introduce bacteria into CSF by doing so * Raised ICP: papilloedema, risk of coning * Shock.

Answer 99

1. Assess GCS: how sick the patient is. The lower the score, the worse they are. Establishes if they can maintain their own airway so if <8, intubate. Assesses if there is any raised ICP. 2. Blood cultures before antibiotics 3. Broad spectrum antibiotics: First line: Cefotaxime or Ceftriaxone because they get through the blood-brain barrier and they are bacteriacidal. Special considerations: Penicillin allergy: 10% chance if they react to penicillin, they will react to cephalosporins. If reaction is usually just a rash, continue. If it is anaphylaxis, give chloramphenicol. Immunocompromised: risk of listeria, add in high dose amoxicillin Recent travel: risk of penicillin resistance. The patient can then be changed to a targeted antibiotic once the cultures are back e.g. for Neisseria give IV benzylpenicillin. 4. Steroids: IV dexamethasone. Reduces the neurological sequelae and therefore reduces morbidity, particularly with strep. Pneuomiae/pneumococcas infection. Prophylaxis for close contacts: • Rifampicin (2 day course, also a TB drug) • Ciplofloxacin (one off). If viral cause, no specific treatment. Just use analgesia, antipyretics and hydration. Aciclovir for herpetic infection. If viral cause, no specific treatment. Just use analgesia, antipyretics and hydration. Aciclovir for herpetic infection.

Answer 100

* Rifampicin (2 day course, also a TB drug) | * Ciplofloxacin (one off).

Answer 101

Chronic autoimmune, T-cell mediated inflammatory disorder of the CNS in which there are multiple plaques of demyelination within the brain and spinal cord, occurring sporadically over years. Repeated episodes if inflammation of nervous tissue in brain and spinal cord.

Answer 102

Women aged 20-40.

Answer 103

Relapsing/remitting MS: most common. Clearly defined disease relapses with full recovery or partial recovery with residual deficits. Periods between disease relapses have no increase in disability between bouts. Primary progressive: disease progression from onset with occasional plateaus and temporary minor improvements but no relapses or remissions. 10-15% of people at onset. Secondary progressive: initial relapsing-remitting disease course followed by continuous progression with or without occasional relapses, minor remissions and plateaus. 50% of those with relapsing/remitting will develop this. Progressive/relapsing: progressive disease from onset, with clear acute relapses with or without full recovery, with periods between relapsed characterised by continuing progression.

Answer 104

Inflammatory process in brain and spinal cord mediated by CD4T cells and B cells. Exposure to EBV in early life predisposes development.

Answer 105

It is a type 4 hypersensitivity reaction (cell-mediated).

Answer 106

Myelin is produced by oligodendrocytes in the CNS. Autoimmune mediated demyelination at multiple CNS sites results in discrete plaques of demyelination which affects the white matter of the brain and specifically the oligodendrocytes. It is thought to be T cell mediated so T cells activate B cells to produce auto-antibodies against myelin. Once T lymphocytes cross the blood brain barrier, they can cause a cascade of destruction to the neuronal cells in the brain. This results in demyelination and loss of myelin sheath along the CNS and therefore conduction is disrupted along axons. This slows/blocks transmission of signal to and from the brain. Although the myelin sheath does regenerate, the new myelin is less efficient and temperature dependant. When exposed to high heat, conduction through new myelin drastically decreases. E.g. if loss of myeline around the optic nerve, vision loss. This will recover after a while but if stress occurs on optic nerve after it’s recovered e.g. hot shower, then blurred vision returns. This is known as Uhtoff’s phenomenon (worsening of neurological symptoms in MS when body gets overheated from hot weather, exercise, saunas and hot tubs). Peripheral nerves are never effected. Plaques of demyelination are perivenular (occur around a vein) and occur everywhere in the CNS but commonly at: • Optic nerves (optic neuritis is often first presentation) • Around ventricles of the brain • Corpus callosum • Brainstem and cerebellar connections • Cervical spinal cord.

Answer 107

Oligodendrocytes in the CNS.

Answer 108

* Pattern 1: macrophage mediated * Pattern 2: antibody mediated. Lots of inflammation, those patients respond to certain therapies such as plasma exchange. * Pattern 3: distal oligodendrogliopathy and apoptosis (ischaemic/toci, virus induced) * Pattern 4: primary oligodendoglia degeneration (metabolic defect).

Answer 109

``` Depends on the region effected. Due to the fact that it is cerebral white matter, Charcot’s neurological triad: • Dysarthria: due to plaques in brainstem. Difficult or unclear speech, can affect eating, talking, swallowing. • Intention tremor: due to plaques along motor pathways. Muscle weakness and spasms, tremors, ataxia, paralysis • Nystagmus: due to plaques in nerves of eye. Loss of vision, optic neuritis, painful eye movements, double vision. Cerebral hemisphere: • Large variety of symptoms by also silent lesions • Depends on which hemisphere. Spinal cord: • Lhermitte’s sign: electric shock runs down back and radiates to limbs • Bladder and sexual dysfunction • Weakness • Paraplegia • Spasticity • Tingling • Numbness. Optic nerves: • Impaired vision • Eye pain. Medulla and pons: • Dysarthria • Double vision • Vertigo • Nystagmus. ```

Answer 110

``` For typical, remember LOSS NB: L hermitte’s sign O ptic neuritis: impaired vision and eye pain S pasticity and other pyramidal signs S ensory symptoms and signs N ystagmus, double vision and vertigo B ladder and sexual dysfunction. ``` Exacerbated by heat e.g. showers, hot weather, saunas (Uhtoff’s phenomenon). Improved by cool temperatures.

Answer 111

Heat e.g. showers. Improved by cool temperatures.

Answer 112

MRI with contrast: active lesions will take up the contrast and appear white in colour.

Answer 113

Gold standard: MRI with contrast: active lesions will take up the contrast and appear white in colour • Two or more lesions disseminated in time and space: need to be sure that it affects two parts of nervous system e.g. brain and spinal cord, optic nerve and brain. More than one attack spaced out in time e.g. optic neuritis last year, now present with weakness in both legs. • Exclusion of conditions giving a similar clinical picture • Lumbar puncture with CSF electrophoresis: as inflammation is confined to the nervous system, inflammatory proteins are found in the CSF not serum. Electrophoresis will show oligoclonal IgG bands which means CNS inflammation • Evoked potentials: e.g. visual evoked potential (VEP), tests how long it takes the impulse to travel. Delayed, visual, brainstem, auditory, somatosensory potentials. E.g. simulate optic nerve and measure time for impulse to go from eye to occipital cortex. As there is demyelination, conduction will be slower. • Bloods: B12, FBC, U&Es, LFTs, TFTs, HIV serology, calcium, glucose.

Answer 114

No cure. Acute attacks (in relapsing-remitting MS): IV methylprednisolone (short course of steroid). Chronic: • First line (frequent relapse): SC beta interferon (CI in pregnancy) and glatiramer acetate. • Second line (disease modifying): IV alemtuzumab (CD52 monoclonal antibody that targets T cells) or IV natalizumab (acts against VLA-4 receptors that allow immune cells to cross the blood brain barrier and therefore reduces the number of cells that can enter the CNS and cause damage). Symptoms management: • Tremor: beta blocker • Muscle spasticity: mild to moderate give oral medications e.g. diazepam, baclofen (GABA analogue that reduces Ca2+ influx). In focal disabling spasticity give peripheral nerve blockers e.g. phenol, alcohol, botulinum toxin. General rehabilitation: • Removal of trigger factors e.g. UTI, bed sores • Physical treatments e.g. physio • Neuropathic pain: gabapentin. Orthotic devices: • Wrist bands containing small weights • Computer controlled mechanical damping devices. Thalamic surgery: • Sterotactic thalamotomy • Thalamic electrostimulation.

Answer 115

McDonald criteria.