Neurology Flashcards

Question

Motor symptoms of parkinsons disease?

Answer 1

- Akinesia - Tremor (typically starts in the fingers, called a pill-rolling tremor – dragging thumb across hand) - Rigidity: can be cogwheel (jerky rigidity associated with tremor) or lead-pipe (smooth, continuous rigidity) - Postural and gait disturbances (stooped posture, shuffling gait (festination), slow turns, freezing and reduced arm swing) - Speech and swallowing difficulties

Answer 2

parkinsons

Answer 3

parkinsons

Answer 4

- Look at features of their gait - Masked like expression due to lack of facial movement - Micrographia (they write really small) - Froment’s manoeuvre – rigidity increases in examined body segment by voluntary movement of contralateral body parts

Answer 5

Parkinson’s Disease causes what is called extrapyramidal symptoms because the symptoms originate out with the pyramidal tract (which allows voluntary movement). There is extra movement that they don’t want and when they do want movement it is slow to initiate.

Answer 6

if suspect parkinsons the person should be referred to a specialist • No lab test that can be used to diagnose, mainly a clinical diagnosis • Dopamine Transporter Imaging using SPECT or PET can be useful to visualise dopamine transporter levels

Answer 7

• First line treatment should be L dopa to anyone who has Parkinson’s disease with motor symptoms affecting quality of life • In those with early stage disease whose motor symptoms are not affecting quality of life could consider a choice of L dopa, dopamine agonists or MAO inhibitors

Answer 8

L dopa is converted in the brain into dopamine. It provides the most improvement in motor symptoms and in activities of daily living. However, this drug causes more motor complications than dopamine agonists, but it does cause less adverse events (although still get adverse events such as excessive sleepiness and impulse control disorders) Motor complications of L dopa include: - Motor fluctuations - Dyskinesias - Need for higher doses to get same effect (because L dopa eventually causes dopamine producing cells to stop working by methylation which is why the dose keeps needing increased and dyskinesia becomes worse) - On/off phenomena where patients go suddenly from mobile to immobile state

Answer 9

Dopamine agonists mimic the effect of dopamine but aren’t actually converted to dopamine like L dopa is. These provide less improvement in motor symptoms and activities of daily living. However, they have fewer motor complications but do cause more adverse events (including excessive sleepiness, hallucinations and impulse control disorders)

Answer 10

These are sometimes used and cause fewer motor complications and fewer adverse events but also less improvements.

Answer 11

Parkinsonism encompasses any condition that causes TRAP (tremor, rigidity, akinesia/ bradykinesia, postural disturbances) which are extrapyramidal symptoms. Parkinsonism can be caused by anything that causes a relative dopamine deficiency in the nigrostriatal pathway. An example would be antipsychotic drugs which block the D2 receptors and therefore can cause parkinsonism as well as other extrapyramidal side effects.

Answer 12

Parkinson’s disease dementia refers to those who develop dementia > 1 year after PD diagnosis. Dementia with Lewy Bodies is dementia as a presenting complaint or within 1 year of PD diagnosis.

Answer 13

lead pipe rigidity is defined as a constant resistance to motion throughout the entire range of movement. Cogwheel rigidity refers to resistance that stops and starts as the limb is moved through its range of motion.

Answer 14

• Most common neuroinflammatory disorder in Western populations (note examples of other neuroinflammatory disorders are post infectious disorders, transverse myelitis etc. these aren’t covered much in curriculum to my knowledge) • T cell mediated disorder • Multiple plaques of demyelination are found throughout the brain and spinal cord occurring sporadically over years

Answer 15

• The condition is more common in women • Typically presents between age 20-40 years • There is a genetic predisposition- if someone in your family has it you have an increased chance of developing the condition

Answer 16

• Plaques of demyelination 2-10mm in size are cardinal features, only effect CNS- peripheral myelinated nerves are not directly affected (hence there are UMN signs NOT LMN) • Plaques can occur anywhere in the CNS but there are sites which are more commonly affected: optic nerves, periventricular region, the corpus callosum, the brainstem, cerebellar connections and the cervical spinal cord • Acute relapses are caused by focal inflammation causing myelin damage and conduction block, recovery follows as inflammation subsides and remyelination occurs • When damage is severe, secondary permanent axonal destruction occurs • Progressive axonal damage is the pathological basis of the progressive disability seen in the progressive forms of MS • Grey matter damage also takes place early on and the extent of the damage correlates with the severity of disability and cognitive involvement

Answer 17

depends on area affected: - pyramidal dysfunction - sensory nerve involvement - cerebellar symptoms - bladder symptoms - optic neuritis - fatigue - compression of cranial nerves in brainstem e.g. 6 and 7

Answer 18

- Painful visual loss in an eye develops over 1-2 weeks - Pain on eye movements - Very rarely complete blindness usually loss of central vision with colour desaturation - RAPD positive (the pupil dilates in response to swinging light test) - Most improve

Answer 19

• At least 2 episodes suggesting demyelination • “Evidence of damage to the CNS that is disseminated in time and space” (i.e. damage that has occurred on different dates and different places) • Blood tests should be done to exclude other inflammatory disorders and infections e.g. borellia, syphilis • MRI is the definitive investigation as it demonstrates areas of demyelination with high sensitivity • Lumbar puncture is abnormal in most patients with MS, there are oligoclonal bands in the CSF with NO corresponding bands in the serum

Answer 20

• RELAPSING AND REMITTING: this is the most common, symptoms occur in attacks which get fully or partially better over weeks, the patient may accumulate disability over time if they don’t fully recover from the relapses • SECONDARY PROGRESSIVE: 75% of people with RRMS evolve into this type within 35 years of onset where they experience gradually worsening disability • PRIMARY PROGRESSIVE: gradually worsening disability without relapses or remissions • RELAPSING PROGRESSIVE: least common type, relapses on a pattern of progressive disability from the outset

Answer 21

referred to specialist for treatment symptom management e.g. bladder training, anticholinergics, physiotherapy, neuropathic pain treatment etc acute exacerbations are treated with observation, oral or iv steroids depending on severity spasticity - baclofen or gabapentin disease modifying drugs: 1st line for RRMS are tecfidera, interferons, glutamir acetate, 2nd line or first for progressive are fingolimid, cladribine, monoclonal antibodies (more effective but more toxic)

Answer 22

• Although people become progressively disabled most people live similar length lives to those without MS • Some rarer aggressive forms may cause death

Answer 23

• An epileptic seizure can be defined as a sudden synchronous discharge of cerebral neurons causing symptoms or signs that are apparent either to the patient or to an observer • Epilepsy is a tendency to recurrent, usually spontaneous epileptic seizures

Answer 24

• Seizures can be classed as focal or general • Focal seizures occur in a focal region of the brain e.g. a focal sensory seizure or a focal motor seizure • General seizures affect the whole brain, there is simultaneous involvement of both hemispheres, always associated with loss of consciousness or awareness

Answer 25

• Focal epilepsy is a type of epilepsy where there is a seizure focus (part of brain that doesn’t work properly) that can irritate the surrounding brain, this focus can cause a focal seizure if the irritation stays in that area or it can cause a general seizure if the abnormal electrical activity hits a cortical network allowing it to spread throughout the brain • In generalised epilepsy the seizures happen on cortical networks so as soon as they occur they immediately propagate around the brain and generalised seizures occur • Focal epilepsy can cause focal or generalised seizures • Generalised epilepsy can only cause generalised seizures

Answer 26

absence, myoclonic, tonic, atonic, tonic clonic

Answer 27

• Loss of awareness and vacant expression <10 secs before returning abruptly to normal and continuing as though nothing happened • Patients are not aware but they could have many of these seizures a day • Patient appears like they are day dreaming/ dozing but they can’t be snapped out of it • May have slight eye fluttering but apart from that there are no motor symptoms

Answer 28

• Jerk movements • Momentary brief contractions of muscles or muscle groups • E.g. involuntary twitch of a finger or hand

Answer 29

• Consists of a stiffening of the body not followed by jerking

Answer 30

• Sudden collapse with loss of muscle tone and consciousness

Answer 31

• Often no warning before these occur • An initial tonic stiffening is followed by the clonic phase with synchronous jerking of the limbs reducing in frequency over about 2 minutes until the convulsions stop • When the convulsions stop there may be incontinence • A period of flaccid unresponsiveness is followed by gradual return of awareness with confusion and drowsiness lasting 15 mins to an hour or longer, headache is common after

Answer 32

the brain is structurally normal tend to present in childhood/ early adulthood 3 main syndromes: childhood absence epilepsy, juvenile myoclonic epilepsy and monogenic epilepsies

Answer 33

absence seizures, spontaneous remission by age 18 is usual

Answer 34

accounts for 10% of all epilepsies, typically myoclonic jerks start in teenage years (which are usually ignored) followed by generalised tonic clonic seizures that bring the teenager to medical attention, seizures and jerks can occur in the morning after wakening, lack of sleep, alcohol and strobe or flickering lights can all be triggers, this type of epilepsy has a good response to treatment but treatment is required lifelong

Answer 35

• Hippocampal sclerosis • Genetic and developmental disorders • Trauma, hypoxia and surgery • Vascular disorders • Infections e.g. encephalitis, cerebral abscess • Alcohol and drugs • Immunological disorders e.g. autoimmune antibody mediated encephalitis or NMDA antibodies

Answer 36

may have an aura or strange feeling, during the seizure they may have convulsions, after the seizure they may have a headache and confusion and take a while to recover, common triggers include strobe or flickering lighting, sleep deprivation, alcohol and drugs

Answer 37

• After a single seizure must tell the patient to stop driving • If patient continues to drive the doctor has the responsibility to inform the DVLA • After a single seizure you are not allowed to drive a motor car for 6 months or a HGV for 5 years • If receive a diagnosis of epilepsy you are not allowed to drive a car until you have been a year seizure free and not allowed HGV until 10 years off all medication and seizure free • If the only type of seizure someone has ever had doesn’t affect consciousness or someone’s ability to drive and the 1st seizure was over 12 months the person can still drive • If the person only ever has seizures at night and the 1st seizure was 12 months ago the person can still drive OR if the person has only had night seizures for the past 3 years

Answer 38

• Sodium valproate is first line monotherapy for boys, men, girls under 10 unlikely to need treatment when old enough to have children, women who are unable to have children • If first line therapy of sodium valproate is unsuccessful try lamotrigine or levetiracetam • Lamotrigine or levetiracetam is first line monotherapy for women and girls of child bearing age or those likely to be on treatment when of child bearing age • Only try sodium valproate for women and girls if discussed pregnancy risks etc

Answer 39

• Lamotrigine or levetiracetam as first line monotherapy, if first choice unsuccessful try the other • Second line choices are: carbamazepine, oxcarbazepine, zonisamide

Answer 40

• First line is sodium valproate but if not suitable then can consider levetiracetam or topiramate

Answer 41

• A number of AEDs are enzyme inducing and can make many forms of contraception including COCP and emergency contraception pills ineffective

Answer 42

carbamazepine

Answer 43

medical emergency • Defined as continuous seizure activity for longer than expected, generally 5 minutes is threshold although previously it was longer (can also be 2 seizures without recovery for similar length of time)

Answer 44

permanent cerebral damage, rhabdomyolysis and AKI

Answer 45

• Severe metabolic disorders • Infection • Head trauma • Sub arachnoid haemorrhage • Abrupt withdrawal of AEDs • Treating absence seizures with carbamazepine

Answer 46

1. Provide resuscitation and immediate emergency treatment for anyone with convulsive status epilepticus (defined as seizures lasting longer than 5 minutes) 2. If the patient has an individualised emergency plan use this 3. If not then give a benzodiazepine (buccal midazolam, rectal diazepam or IV lorazepam if IV access) 4. Wait five minutes, if not stopped give a second dose 5. Wait five minutes, if not stopped, second line treatment is IV levetiracetam, phenytoin or sodium valproate 6. If not stopped, consider other second line treatments 7. Third line treatments are phenobarbital or general anaesthesia  You should also be looking for underlying causes and if can treat these  Do NOT give more than 2 doses of benzodiazepine as this could cause respiratory arrest  Any suggestion of hypoglycaemia give IV glucose  Any suggestion of alcoholism or impaired nutritional status give thiamine  Once status is stabalised a person should be put back on their usual anti-convulsant drugs  Most acute seizures stop themselves so it is only status epilepticus that needs treated

Answer 47

• Any new onset headache in someone over 55 • Anyone with known/ previous malignancy • Anyone immunosuppressed • Early morning headache • Associated with nausea and vomiting • Headache that wakes you up • Headache that is exacerbated by the valsava manuovre or leaning forward • Visual symptoms

Answer 48

5 attacks lasting 4-72 hours may experience aura pain is unilateral pulsating quality moderate or severe pain intensity aggravated by routine activities nausea and/ or vomiting photophobia or photophobia

Answer 49

visual e.g. scotomas, central fortification, hemianopia, sensory or motor disturbances, there is separate criteria for diagnosis These auras usually last 20-60 minutes and are followed by the headache phase

Answer 50

sleep deprivation, skipping meals, alcohol, hormones (oestrogen), physical exertion

Answer 51

• Non-pharmacologic treatment: headache diary, education on avoiding triggers, relaxation, stress management • Acute abortive treatments include high dose NSAIDs e.g. naproxen, triptans are specific for migraines and these can be effective where NSAIDs are insufficient e.g. sumatriptan, almotriptan. It should be noted that overuse of acute abortive treatments can lead to dependence and cause further headaches • Suppression medication can be used when migraine episodes are frequent (more than 1-2 per month) and impacting on quality of life. amitriptyline or propranolol or topiramate

Answer 52

tension headache

Answer 53

• Pain is usually mild to moderate, bilateral, tight band sensations, pressure behind the eyes, bursting sensation • There is the absence of photophobia, phonophobia, nausea and vomiting

Answer 54

simple analgesics are often enough Scalp relaxing treatments e.g. massage and ice packs can help Tricyclics may be used for chronic case

Answer 55

Trigeminal Autonomic Cephalgias are a group of primary headache disorders characterised by unilateral trigeminal distribution of pain (usually in the ophthalmic division of the nerve) and prominent ipsilateral autonomic features. This group encompasses four primary headache disorders e.g. cluster headaches, paroxysmal hemicrania, hemicrania continua and SUNCT.

Answer 56

• There is excruciating unilateral headache with parasympathetic autonomic activation in the same eye causing redness or tearing, nasal congestion or even a transient Horner’s syndrome • Frequency of attacks is 1-8 a day, lasting 45-90 minutes, with bouts lasting 1-2 months • Bouts usually recur a year or more later often at the same time of year

Answer 57

males age 20-40

Answer 58

• High flow O2 100% helps acutely and so does subcutaneous sumatriptan (no other drugs work quickly enough) • Verapamil or steroids may help terminate a bout of cluster headaches

Answer 59

elderly women

Answer 60

• The headaches have same features as cluster headaches but are of shorter duration than cluster headaches but tend to occur more frequently • They usually last 10-30 mins and there is 1-40 a day

Answer 61

indomethacin

Answer 62

• Stands for short lasting unilateral neuralgiform headache with conjunctival injection and tearing • Attacks are very short lasting 5 seconds to 2 minutes and often occur in bouts

Answer 63

involves IV lidocaine for acute attacks or prevention with lamotrigine or gabapentin

Answer 64

• Typically develops in younger, overweight females many of whom have polycystic ovaries

Answer 65

Features include those of raised intracranial pressure e.g. headache worse in morning, headache with nausea and vomiting, headache with visual obscurations due to papilloedema

Answer 66

• MRI is usually normal • Lumbar puncture shows elevated CSF pressure but normal constituents

Answer 67

• Treatment involves monitoring visual fields, encouraging weight loss, acetozalmide and thiazide diuretics can be used to reduce CSF production • Sometimes ventriculoperitoneal shunt insertion or optic nerve sheath fenestration to protect vision is sometimes necessary

Answer 68

more common in elderly hypertension is the main risk factor

Answer 69

• It is often due to compression of the trigeminal nerve at or near the pons by ectatic vascular loop (can be seen on high resolution MRI)

Answer 70

• It causes severe sharp, stabbing unilateral pain in the fifth nerve distribution lasting seconds but attacks occur 10-100x a day • Can be caused by trivial stimuli such as washing, shaving or chewing • Bouts of pain can last weeks to month

Answer 71

Carbamazepine reduces the severity of attacks, can do ablation or decompression of the blood vessel if very severe

Answer 72

• Auto-immune disorder of the neuromuscular junction transmission • Antibodies to acetylcholine receptor protein are present and these form complexes which cause destruction of the acetylcholine receptors which blocks binding of Ach to the post synaptic membrane • As Ach is the NT at the NMJ this means signals don’t get through to the muscle • Symptoms start when Ach receptors are reduced to 30% of normal

Answer 73

females in 2nd and 3rd decade males in 6th and 7th decade

Answer 74

• There is a strong association with thymic abnormalities and thymic hyperplasia is found in 70% of MG patients under the age of 40 (this kind of make sense because the thymus is involved in the immune response) • In a smaller amount of patients a thymic tumour may be found • There is also an association between MG and other autoimmune diseases

Answer 75

• Weakness that worsens throughout the day – fatigability • Most commonly there is extraocular, facial and bulbar weakness (can also get proximal limb weakness) • Drooping eyelids • There are usually eye movement abnormalities and the patient may complain of double vision that comes and goes

Answer 76

• Check for positive serum anti-AchR and anti-MuSK antibodies (present in varying percentages of cases depending on type of MG) • Repetitive nerve stimulation test shows characteristic decrements in evoked muscle action potential during repetitive stimulation • Imaging to look for thymic abnormalities (CT)

Answer 77

• Acute treatment: acetylcholinesterase inhibitors (allows persistence of Ach so get transmission), IV immunoglobulin • Steroids are initially given at diagnosis but then moved slowly to steroid sparing agents e.g. azathioprine and mycophenolate

Answer 78

gentamicin

Answer 79

• MG fluctuates in severity and is a lifelong illness- there is a low mortality of 3-4%

Answer 80

• Sudden worsening of symptoms, may or may not have triggers • Often involves acute respiratory failure due to weakness of the muscles of respiration • Characterised by FVC below 1L, negative inspiratory force (NIF) of 20cm H2O and the need for ventilatory support • Weak cough may indicate weakness of expiratory muscles • 2 main treatments involve IV immunoglobulin and plasma exchange

Answer 81

ischaemic (85%), haemorrhage (15%)

Answer 82

• Ischaemic strokes are mainly due to atherosclerotic plaques (thrombus) causing vessel occlusion or cardioemboli (embolus comes from the heart) which are commonly caused by AF • Some cause of haemorrhagic strokes include structural abnormalities, hypertension, amyloid angiopathy or a combination of these factors

Answer 83

• This includes infarcts in the territory of the internal carotid, middle cerebral artery, anterior cerebral artery and ophthalmic arteries • A total anterior circulation infarct (TACI) consists of all three of: higher cerebral dysfunction (higher cerebral function is anything conscious controlled by cerebrum e.g. dysphasia), homonymous visual field defect and ipsilateral motor and/ or sensory deficit in at least 2/3 of face, arms or legs • A partial anterior circulation infarct (PACI) consists of only 2/3 of a TACI

Answer 84

• These are small infarcts presumed to result from the occlusion of a single small perforating artery supplying the subcortical areas of the brain • It is defined as a pure motor or sensory stroke or an ataxic hemiparesis (ataxic weakness on one side of the body)

Answer 85

• Posterior circulation infarcts involve vertebral, basilar, posterior cerebral or posterior communicating artery • It is defined as one of: Ipsilateral cranial nerve palsy with contralateral motor and/or sensory deficit, bilateral motor and/or sensory deficit, cerebellar dysfunction, isolated homonymous visual field defect

Answer 86

• Speech: dysarthria, dysphasia • (Note dysarthria is speech disorder caused by impairment of muscle control, dysphasia is impairment of language) • Facial weakness: stroke can affect the UMN of cranial nerve 7 which supplies the muscles of facial expression, the facial nerve receives bilateral cortical innervation to the upper part of the face (raising eyebrows) but unilateral to the lower part of the face, so someone with a stroke affecting the facial nerve may not be able to smile on the affected side but will be able to raise their eyebrows and close their eyes • Contralateral limb weakness and sensory loss • Cerebellar signs

Answer 87

non contrast ct

Answer 88

• Haemorrhage is demonstrated immediately on CT as a white area (acute blood appears white on non contrast CT) • Very early findings of an ischaemic stroke may be a hyperdense segment of a vessel (direct visualisation of thrombus) • Within the first few hours there is loss of grey white matter differentiation, cortical hypodensity with associated parenchymal swelling and effacement of gyri • Within time the swelling becomes more marked and there is mass effect • Eventually gliosis occurs and there is a low density region visible with volume loss

Answer 89

alteplase 4.5 hours

Answer 90

less treatment available, aggressively manage any hypertension with IV GTN to lower BP as this has been shown to improve outcomes

Answer 91

• There is transient obstruction of blood flow to the brain, spinal cord or retina causing a sudden onset of symptoms that typically last for minutes to an hour (timeframe of less than 24 hours isn’t used anymore) • There is complete recovery and no evidence of infarction on imaging • Hemiparesis and aphasia are the most common symptoms

Answer 92

sudden transient loss of vision in one eye and is a type of stroke

Answer 93

• Lifestyle measures: encourage physical activity every day, advice on stopping smoking, healthy diet, keep alcohol consumption within recommended limits • Antiplatelet therapy usually clopidogrel (aspirin for 2 weeks, clopidogrel life long) • Statin • Anti-hypertensives • Anticoagulants for those with AF • Optimise treatment of any other conditions the person has that could affect stroke risk e.g. diabetes, heart failure

Answer 94

the facial nerve receives bilateral cortical innervation to the upper part of the face (raising eyebrows) but unilateral to the lower part of the face, so someone with a stroke affecting the facial nerve may not be able to smile on the affected side but will be able to raise their eyebrows and close their eyes

Answer 95

rupture of intracranial berry aneurysm

Answer 96

• These aneurysms form due to congenital weakness of the elastic tissues in the arterial wall, incidence of haemorrhage increases with age, hypertension is an important contributing factor • Aneurysms often develop near arterial junctions in the Circle of Willis • The prevalence of berry aneurysms in the population is estimated at about 3%, so there will be many people with these aneurysms who never know and never have any problems • Factors that make berry aneurysms more likely to rupture include: smoking, hypertension, location of aneurysm, size of aneurysm, conditions such as polycystic kidney disease where aneurysms are both more common and likely to rupture

Answer 97

AVM and bleeding disorders

Answer 98

• Sudden onset of “thunderclap headache” patients claim it is the worst headache of their life • Neck stiffness and photophobia due to meningeal irritation • Headache is often accompanied by nausea or vomiting due to increased ICP or meningeal irritation • If the aneurysm is of the posterior communicating artery then a third nerve palsy may occur • Sometimes confusion, seizures and loss of consciousness can occur • Sometimes can get vitreous haemorrhage associated with SAH

Answer 99

• Diagnosis is usually confirmed with an unenhanced CT scan where a large volume of acute blood which appears white is seen in the suprasellar cistern, sylvian fissures and sulci • Lumbar puncture may be performed if doubt remains after CT and would be checking the CSF for signs of blood • When SA blood is found in the absence of a history of trauma CT cerebral angiography is performed to look for the underlying berry aneurysm

Answer 100

• Immediate treatment of SAH involves bed rest and supportive measures. Hypertension should be controlled. Nimodipine, a calcium-channel blocker given for 3 weeks, reduces mortality • Nearly half of SAH cases are either dead or moribund before reaching hospital. Of the remainder, a further 10–20% rebleed and die within weeks. Failure to diagnose SAH – for example, mistaking SAH for migraine – contributes to this mortality • Where angiography demonstrates an aneurysm (the cause of the vast majority of SAHs), endovascular treatment by placing platinum coils via a catheter in the aneurysm sac, to promote thrombosis and ablation of the aneurysm, is now the first-line treatment • Endovascular coiling has a lower complication rate than surgery but direct surgical clipping of the aneurysm neck is still required in some selected cases

Answer 101

Vasospasm as blood in SA space irritates vessels and can then get ischaemia - nimodipine used to prevent spasm re-bleeds are common hydrocephalus seizures hyponatraemia (causes SIADH)

Answer 102

Acute is due to high impact head trauma which results in rupture of the bridging veins chronic SDH is associated with brain atrophy due to age, chronic alcoholism or dementia resulting in stretched bridging veins which rupture with even small amount of trauma and blood slowly accumulates in SD space

Answer 103

non contrast CT

Answer 104

• May not need immediate treatment but it is important to involve neurosurgery • Even large collections can resolve on their own • Serial imaging is required to assess progress • If needed they can be drained surgically

Answer 105

from the middle meningeal artery from a temporoparietal fracture because the artery runs under the thinnest part of the skull called the pterion

Answer 106

• Typically presents in a young adult after head trauma • Classically presents with a brief loss of consciousness, followed by a lucid interval after that the patient further deteriorates, exhibiting symptoms such as headache, vomiting, contralateral hemiparesis (stalks that attach the cerebrum to the brainstem and contain a lot of the ascending and descending tracts) and ipsilateral pupillary dilatation (due to temporal lobe herniating and compressing the oculomotor nerve)

Answer 107

• Expanding extradural haematomas need immediate neurosurgical evacuation • Conservative management is sometimes considered in neurologically intact patients with small haematomas

Answer 108

Strep pneumonia and neisseria meningitidis (meningococcus)

Answer 109

negative pairs

Answer 110

neisseria meningitidis

Answer 111

there are 12 capsular groups of meningococcus and the vaccine is for ACWY

Answer 112

blood stream infection with meningococcus so you can have meningitis and no rash because its a different organism or can have meningococcus infection but not meningitis and have the rash

Answer 113

postive chains

Answer 114

strep pneumonia

Answer 115

only really causes illness in neonates, elderly and immunosuppressed particularly those with malignancy

Answer 116

• This causes a chronic meningitis more common in areas with lots of TB • Generally, it causes non-specific ill health • This is treated similarly to pulmonary TB with rifampicin, isoniazid, ethambutol and pyrazinamide

Answer 117

• Headache • Neck stiffness • Fever • Photophobia • Vomiting • Intense malaise • Petechial rash in meningococcal infection

Answer 118

• This is almost always a benign self-limiting condition lasting 4-10 days • Headache may follow for some months • There are no serious sequelae unless an encephalitis is present

Answer 119

CRP and WBC PCR tests from blood samples throat swab for culture CSF sample from lumbar puncture can be done as a primary investigation unless contraindicated

Answer 120

viral meningitis

Answer 121

tuberculosis meningitis

Answer 122

• Ceftriaxone IV 2g bd (if penicillin allergic can give chloramphenicol) + dexamethasone just before or started with antibiotics • If listeria is suspected then must give amoxicillin too because ceftriaxone does NOT cover listeria • Listeria should be suspected in anyone 60 or over and anyone immunocompromised (immunocompromised includes those with alcohol dependency and those with diabetes) • If there has been travel in the last 6 months to a country with high rates of penicillin resistance then vancomycin should be added

Answer 123

• Public health must be informed of every suspected case of bacterial meningitis • May do tracing and give prophylactic treatment to contacts

Answer 124

• Mainly symptomatic treatment • May give antivirals depending on causative organisms etc

Answer 125

mainly due to viral infection • Most common cause in the UK is the herpes simplex virus • Other causes include: measles, mumps, rubella, varicella zoster, enteroviruses and adenoviruses

Answer 126

• Insidious onset (gradual and subtle but harmful) • Personality and behavioural changes • Confusion and speech disturbance • Reduced consciousness • Coma • Focal neurological deficits • Seizures

Answer 127

• MRI shows areas of inflammation and swelling (bright areas), raised ICP and midline shift may occur • EEG shows periodic sharp and slow wave complexes • CSF shows elevated lymphocyte count • Viral detection by CSF PCR can detect HSV or VZV

Answer 128

• Suspected VZV or HSV encephalitis is treated immediately with IV acyclovir even before investigation results are available • (measles, mumps, rubella and other less common causes are treated differently) • Early treatment significantly reduces both mortality and long term neurological damage in survivors • Seizures are treated with anticonvulsants • Long term complications are common and include memory impairment, personality change and epilepsy

Answer 129

no they are 10 times rarer than brain tumours

Answer 130

• Abscesses may occur due to trauma from neurosurgery, spread from dental infection or spread from ENT infection • Common bacteria are strep viridans and Bacteroides species (from paranasal sinuses and teeth) and staphylococci from penetrating trauma • Mixed infections are common • In immunocompromised should consider toxoplasma and fungal sources

Answer 131

headache, focal signs, hemiparesis, hemianopia, epilepsy and signs of raised intracranial pressure

Answer 132

• May have fever, leukocytosis and raised ESR • MRI shows a ring enhancing mass usually with considerable surrounding oedema • Lumbar puncture is dangerous and should not be performed • Neurosurgical aspiration with stereotactic guidance allows the infective organism to be identified

Answer 133

• Treatment is with high dose antibiotics and sometimes surgical resection/ decompression • Despite treatment, mortality remains high at approximately 25%, epilepsy is common in survivors

Answer 134

• Acute weakness or paralysis of the muscles of the face due to idiopathic damage to 7th cranial nerve, LMN lesion • Thought to be due to association with HSV, EBV, VZV viral infections • Fairly common

Answer 135

• Unilateral facial weakness develops over 24-48 hours • Absence of nasolabial fold, drooping of eyelid and of mouth, dryness in affected eye or mouth, hypersensitivity to loud noise and loss of taste on ant 2/3 • It is important to distinguish this from an UMN lesion e.g. a stroke, in a UMN lesion the patient will only have paralysis of their lower face as UMN innervation is bilateral to the upper part of the face but unilateral to the lower

Answer 136

• Need to determine that the problem is ONLY with the facial nerve (if others involved it is not Bell’s palsy) and is LMN lesion • Diagnosis is made on clinical grounds and tests are generally not needed

Answer 137

• In general, most recover within 3-6 months without specific treatment • Patients should be reassured that prognosis is good and it is unlikely to recur • Inability to blink can lead to exposure keratitis and patients may need lubricating eye drops and advised to tape eyes shut at night • Early treatment with corticosteroids can improve outcomes if started within 72 hours

Answer 138

• Pyramidal pattern of weakness – naturally the flexors in the upper limb are strong and the extensors are strong in the lower limb – evolutionary - we want to be able to lift our hands up to protect our face and extend our legs to stand up straight • A pyramidal pattern of weakness involves weak flexors in the upper limb and weak extensors in the lower limb

Answer 139

raccoon eyes, CSF rhinorrhoea, battle sign, haemotympanum, raccoon eyes, CSF rhinorrhoea, battle sign, haemotympanum

Answer 140

unrousable unconsciousness

Answer 141

• Cushing’s reflex = High BP and low HR (you raise your BP really high to perfuse the brain but then because your BP is so high you get reflex bradycardia) • Cushing’s reflex is common in young people with a large extradural haematoma

Answer 142

• Essential tremor aka benign or familial tremors • Cause is unknown but seem to be autosomal dominant • Usually involves tremor in arms, hands or fingers

Answer 143

• Essential tremors are generally postural – present with sustained muscle tone - i.e. when you are holding your arms out • This is in contrast to Parkinsons tremor which occur at rest and cerebellar which occur on action

Answer 144

• Umbrella term encompassing disparate disorders that are apparent at birth or in childhood and are characterised by non-progressive motor deficits • Non progressive disease – single insult – doesn’t get worse or better over time • A variety of intrauterine and neonatal cerebral insults may cause CP including prematurity ad its complications, hypoxia, intrauterine infections and kernicterus (high bilirubin causes brain damage) • In many, cases no specific cause can be identified

Answer 145

• Failure to achieve normal milestones is usually the earliest feature • Specific motor features usually become apparent later in childhood • 70% will have spastic CP • Co-morbidity is common – particularly epilepsy and learning disabilities

Answer 146

• MDT approach – physiotherapy, SALT, OT • Botox injections to relax muscles • Baclofen or diazepam for muscle stiffness • Melatonin for sleeping difficulties • Analgesia for pain • Surgery if needed

Answer 147

• Hypoxic ischaemic encephalopathy is brain injury due to lack of oxygen in the infant’s brain • It can cause cerebral palsy or it can cause cognitive impairments, vision, hearing and motor issues • Cerebral palsy is characterised by lack of motor function and often arises in children whose HIE has affected areas in brain responsible for motor control

Answer 148

a process affecting several individual nerves e.g. you have a neuropathy affecting femoral nerve then median nerve etc

Answer 149

peripheral nerve compression/ entrapment e.g. carpal tunnel syndrome, cubital tunnel syndrome, radial nerve entrapment

Answer 150

• Diabetes mellitus • Leprosy • Vasculitis • Amyloidosis • Malignancy • Neurofibromatosis • HIV and Hepatitis C • Multifocal motor neuropathy

Answer 151

good glycaemic control

Answer 152

guillain barre syndrome

Answer 153

unknown but thought to be related to immune reaction post infection generally campylobacter jejune or CMV

Answer 154

• Weakness of the distal limb muscles and/or distal numbness • Weakness and sensory loss progress over days to 6 weeks • Loss of tendon reflexes almost always occurs paralysis can rapidly progress and can affect rest muscles so prompt treatment and recognition needed

Answer 155

Iv immunoglobulin

Answer 156

Group of hereditary motor and sensory neuropathies get high arched foot

Answer 157

• A radiculopathy is a conduction block in the axons of a spinal nerve or its roots, with impact on motor axons causing weakness and on sensory axons causing paraesthesia and/ or anaesthesia

Answer 158

• Radiculopathy = a state of neurological loss and may or may not be associated with radicular pain • Radicular pain = pain deriving from damage or irritation of the spinal nerve tissue, particularly the dorsal root ganglion

Answer 159

• Intervertebral disc prolapse: the lumbar spine is predominantly affected by repeated minor stresses that predispose to rupture of the annulus fibrosus and sequestration of disc material (the nucleus pulposus) • Degenerative diseases of the spine: leading to neuroforaminal or spinal canal stenosis, the cervical spine is the most mobile segment of the spine and degenerative change is a normal part of the ageing process • Fracture: either trauma or pathological • Malignancy: most commonly metastatic • Infection: such as extradural abscesses, osteomyelitis (most commonly TB), or herpes zoster

Answer 160

• Sensory symptoms in the corresponding dermatome and weakness in the corresponding myotome • Sensory features are paraesthesia and numbness and motor features are weakness • Radicular pain is often also present, typically described as a burning, deep, strap-like, or narrow pain, it is not uncommon for radicular pain to be intermittent • Important to ask about red flag symptoms for cauda equina

Answer 161

• Definitive long term management depends on the underlying cause • In general the only condition that requires emergency surgical treatment is cauda equina syndrome • Most IV disc prolapses can be managed non-operatively, but indications for surgical treatment include unremitting pain despite non-surgical management, progressive weakness, and new or progressive myelopathy (compression of the spinal cord) • Symptomatic management is with analgesia, amitriptyline is usually first line or pregabalin and gabapentin as alternatives, if the patient suffers from muscle spasms these can be managed with benzodiazepines or baclofen, physiotherapy is an important part of management

Answer 162

Spinal: supraspinous ligament interspinous ligament ligamentum flavum epidural space (fat and veins) dura mater arachnoid mater finally reaches subarachnoid space (contains CSF) Epidural: supraspinous ligament interspinous ligament ligamentum flavum epidural space (fat and veins)

Answer 163

refer to a specialist for diagnosis and management

Answer 164

pramipexole, ropinirole, rotigotine and apomorphine, cabergoline, bromocriptine

Answer 165

This is a rare condition where the neurones of multiple systems in the brain degenerate. It affects the basal ganglia as well as multiple other areas. The degeneration of the basal ganglia lead to a Parkinson’s presentation. The degeneration in other areas lead to autonomic dysfunction (causing postural hypotension, constipation, abnormal sweating and sexual dysfunction) and cerebellar dysfunction (causing ataxia).

Answer 166

no cure - tends not to respond as well to levodopa as parkinsons does

Answer 167

baclofen then try gabapentin