neurology Flashcards

Question

symptoms/signs for TIA

Answer 1

* Report of neurological deficit * Bried duration of symptoms * History of cardiac disease * Unilateral symptoms  TIAs represent ischaemia in an are of brain controlling function on the contralateral side of the body * Increased BP on presentation * Absence of headache, shaking, scotoma, spasm, migraine, seizure prior to neurological deficit

Answer 2

* Hypoglycaemia * Seizure with post-seizure (Todd’s) paralysis * Complex migraine * Conversion disorder * MS * Peripheral neuropathy

Answer 3

• 1st LINE: - BLOOD GLUCOSE: hypoglycaemic events can elicit global symptoms such as confusion or syncope, can mimic TIA  blood glucose <3.3 suggests hypoglycaemia as mimic of TIA - CHEMISTRY PROFILE: severe hyponatraemia can trigger seizure or induce generalised weakness  very low sodium, potassium or high calcium suggests non-ischaemic cause of symptoms - FBC: elevated WBC can suggest infection  usually normal - PROTHROMBIN TIME, INR AND ACTIVATED PTT: this is used if the neurological deficit persist at time of presentation, there is reason to suspect abnormal coagulation (liver disease or use of anticoagulant therapy) and thrombolytic therapy for stroke is being considered - ECG: evaluate for AF and other arrhythmias  AF may be present - BRAIN MRI WITH DIFFUSION: half will have positive diffusion images - FASTING LIPID PROFILE: all pts should be treated with statin therapy unless contraindications are present

Answer 4

• 1ST LINE: - ANTIPLATELET THERAPY: aspirin 300mg o + statin: atorvastatin

Answer 5

Prognosis - most significant risk to the pt is a second ischaemic event causing permanent disability Complications - stroke, MI

Answer 6

• Bleeding into the subarachnoid space – the area between the arachnoid membrane and the pia mater surrounding the brain

Answer 7

* Accounts for 5% of strokes * Incidence of 6 per 100,000 per annum. • Mean age of presenting pts is 50

Answer 8

• Spontaenous arterial bleeding into the subarachnoid space • Can be caused by: o Saccular ‘Berry’ Anuerysms (70% of cases)  acquired lesions that are most commonly located at the branching points of the major arteries coursing through the subarachnoid space at the base of the brain (circle of willis) o Congenital arteriovenous malformations (10%) o No lesion can be found in 20% of cases

Answer 9

* Hypertension * Diabetes * Anticoagulation

Answer 10

* Thunderclap headache (being kicked in the head)  pulsates towards the back of the head * Vomiting * Seizures * Confusion * Neck stiffness * Hemiparesis (weakness of one side of the body) * Head injury

Answer 11

* Signs of meningeal irritation  neck stiffness and positive kernings sign * Focal neurological signs * Subhyaloid haemorrhages (between the retina and vitreous membrane) with or without papilloedma * Warning headache a few days before the bleed

Answer 12

* Migraine * Aneurysm * Trauma * Seizure * Hypoglycaemia * Mass lesions

Answer 13

• 1st LINE: - IMMEDIATE CT: shows subarachnoid or intravascular blood in 95% of cases when the scan is done in 24hrs o + lumbar puncture indicated if there is a strong clinical suspicion of SAH but the CT scan is normal  increase in pigments (bilirubin and/or oxyhaemoglobin released from lysis and phagocytosis of RBCs) is the key finding to support SAH, must be performed at least 12hrs after onset and can be detected up to 2 weeks after onset - MR ANGIOGRAPHY: performed to establish the source of bleeding in all pts potentially fit for surgery

Answer 14

prognosis is poor | complications include re-bleeding

Answer 15

• 1st LINE: - ANTI-HYPERTENSIVES: ramipril or calcium channel blocker (depending on race and if over 55) - CALCIUM CHANNEL BLOCKER: nimodipine can be given to reduce cerebral artery spasm - SURGERY: obliteration of the aneurysm by surgical clipping or insertion of a fine wire coil under radiological guidance prevents re-bleeding

Answer 16

• Lymphadenopathy (swelling) of the cervical lymph nodes (glands in the neck)

Answer 17

• Common presentation in infection and in malignancy

Answer 18

* 6 principles that cause nerves to malfunction  demyelination, axonal degeneration (due ot a toxin), Wallerian degeneration following nerve section, compression, infarction (in arteritis) and infiltration by inflammatory cells (e.g. sarcoid) * MONONEUROPATHY = process affecting a single nerve, may be the result of acute compression particularly where the nerves are exposed anatomically (common peronaeal) or entrapment, particularly where the nerve runs through a relatively narrow anatomical passge (carpal tunnel) * MULTIPLE MONO-NEUROPATHY/MONONEURITIS MULTIPLEX = affects several or multiple nerves, often indicates a systemic disorder, treatment is that of the underlying disease, acute presentation is most commonly due to vasculityis when prompt treatment with steroids may prevent irreversible nerve damage * POLYNEUROPATHY = acute or chornic, diffuse, usually symmetrical disease, may involve motor, sensory and autonomic nervesm either alone or in combination, sensory symptoms include numbness, tingling ‘pins and needles’, pain in the extremities and unsteadiness on the feet, numbness tends to affect distal arms and legs in a ‘glove and stocking distribution’, motor symptoms are usually those of weakness, autonomic neuropathy causes postural hypotension, urinary retention, erectile dysfunction, diarrhoea, diminished sweating, impaired puoillary response and cardiac arrhythmias, many varities of neuropathy affect autonomic function to some degree, but occasionally autonomic features predominate  occurs in diabetes, amyloidosis and guillian-barre syndrome • CAUSES: (DAM IT BITCH) - D Drugs and chemicals (Pb, phenytoin, metronidazole, amiodarone, hydralazine, vincristine, isoniazid, organic solvents, sulphonamides, nitrofurantoin, CO, OPs) - A alcohol (with or without Thiamine deficiency) - M metabolic (diabetes, hypoglycaemia, uraemia) - I infection (HIV, leprosy, lyme, diptheria, syphilis) or post infectious (GBS) - T tumour (paraneoplastic phenomenon – lung, lymphoma, myeloma) - B B12 & other vitamin deficiency states, as well as pyridoxine excess - I idiopathic and infiltrative (e.g. amyloidosis) - T toxins (botulism, ciguatera, Tetrodotoxin, Saxitoxin, BRO, tick paralysis) - C connective tissue diseases (e.g. SLE, PAN, RhA) and congenital (e.g. CMT) H Hypothyroidism

Answer 19

* Diabetes * Alcohol abuse * Vitamin deficiencies * Infections e.g. lyme disease, shingles, Epstein-barr virus, hepatitis B and C

Answer 20

* SENSORY NEUROPATHY: pins and needles in the affected body part, numbness and less ability to feel pain or changes in temperature, particularly in your feet, a burning or sharp pain, usually in the feet, feeling pain from somethingthat should not be painful at all, such as a very light touch, loss of balance or co-ordination caused by less ability to tell the position of the feet or hands * MOTOR NEUROPATHY: twitching and muscle cramps, muscle weakness or paralysis affecting one or more muscles, thinning (wasting) of muscles, difficulty lifting up the front part of your foot and toes, particularly noticeable when walking (foot drop) * AUTONOMIC NEUROPATHY: constipation or diarrhoea, particularly at night, feling sick, bloating and belching, low BP which can make you feel faint or dizzy when you stand up, rapid HR, excesive sweating, erectile dysfunction, urinary retention, loss of bowel control

Answer 21

* Diabetes * Trauma * MS * Cord compression * Brain lesion

Answer 22

• 1ST LINE: Bloods - FBC, U&E’s, CRP/ESR, LFTs - SERUM VIT B12 - NERVE CONDUCTION TEST: measures the speed and strength of the nerve signal - ELECTROMYOGRAPHY (EMG): where a small needle is inserted through your skin into your muscle and used to measure the electrical activity of your muscles - EMG AND NCS DONE AT THE SAME TIME

Answer 23

management and prognosis are dependant on the cause complications include gangrene, diabetic foot ulcer, heart and blood circulation problems

Answer 24

• A seizure is defined as a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain • Considered to be a disease of the brain defined by any of the following conditions: 1. At least 2 unprovoked (or reflex) seizures occurring more than 24 hours part 2. One unprovoked (or reflex) seizure and a probability of further seizures similar to the general recurrence risk (at least 60%) after 2 unprovoked seizures, occurring over the next 10 years 3. Diagnosis of an epilepsy syndrome

Answer 25

* 1 in 103 people. 600,000 taking antiepileptic medication * Most commonly starts in children or in people older than 60 (bimodal incidence) * Epilepsy is much more common in people with a learning disability * Epilepsy is often misdiagnosed (20-31% of the time) (usually falsely told they have epilepsy)

Answer 26

* About two thirds of people in the UK do not have an anatomically identifiable cause = idiopathic epilepsy and is the most common cause of epilepsy in younger people * Underlying this is thought to be complex developmental abnormalities in synaptic connections and neurotransmitter distribution and release * A genetic predisposition is involved in many people – about 30% of people with it have a first degree relative with it • Another third have an identifiable anatomical abnormality (this tends to be in the older age group) = symptomatic epilepsy and is caused by cerebral vascular disease, cerebral tumour and post-traumatic epilepsy, less common identifiable causes include perinatal brain injury caused by foetal hypoxia or trauma, cortical or vascular malformation, cerebral abscess or tuberculoma and surgery to the brain

Answer 27

* Fx * Genetic conditions – childhood epilepsy syndromes, or neurocutaneous syndromes such as TB sclerosis or neurofibromatosis * Previous febrile seizure (2-7%) * Previous intracranial infections * Brain trauma esp. penetrating or surgery * Comorbid conditions such as CVD or cerebral tumours

Answer 28

• SPECIFIC FEATURES OF GENERALISED SEIZURES: - TONIC  impairment of consciousness and stiffening (trunk straight or flexed at waist) - CLONIC  jerking and impairment of consciousness - TYPICAL ABSENCE SEIZURES  which begin in childhood, sharp onset and no residual symptoms, normal activity is interrupted ad the child stares for a few seconds, eyelids may twitch and some very small jerking movements of the hands may occur, lasts 5-10 seconds and usally less than 30, can occur hundreds of times a day in children - MYOCLONIC  brief, shock-like contraction of the limbs without the apparent impairment in consciousness - ATONIC  sudden brief attacks of loss of tone, associated with falls and LOC • SPECIFIC FEATURES OF FOCAL SEIZURES: - FOCAL MOTOR  jerking movement, typically beginning in the face or one hand, and spreading ot involve the limbs, may also present with apparent purposeful movements such as turning the head, eye movements, lip smacking and mouth movements, drooling, or rhythmic muscle contractions, limb weakness may occur for several hours after the seizure - FOCAL SENSORY  include temporal lobe seizures that may cause sensory, autonomic, emotional, cognitive or other changes • Secondary generalised seizures start with a focal seizure before spreading to cause a generalised seizure • Possibly with symptoms of auras (simple partial seizures, no LOC), particularly those arising in the temporal lobe, these include symptoms of unexpected tastes, smells, paraesthesia or rising abdominal sensation

Answer 29

* Syncope (e.g. caused by postural changes) * Cardiac arrhythmias * Panic attacks with hyperventilation * Non-epileptic attack disorders * In children between 6 months and 5 years: night terrors, breath holding attacks, stereotyped behavioural phenomena and masturbation – especially in those with a learning disability

Answer 30

* Lymph node examination * If unexplained  consider a very urgent FBC * In people >40, with supraclavicular lymphadenopathy or persistent cervical lymphadenopathy, consider an urgent chest X-ray

Answer 31

• 1st LINE: - TONIC CLONIC: if less than 5 minutes  protect pt and do not restrain, if morenthan 5 minutes  buccal midazolam (1st line in community), rectal diazepam (2nd line when buccal midazolam is not available), IV lorazepam if IV access is established and resuscitation facilities available - STATUS EPILEPTICUS: buccal midazolam (1st line in community), rectal diazepam (2nd line when buccal midazolam is not available) - PREVENTION: drugs given to prevent an attack are specific for the type of seizure  TONIC CLONIC = sodium-valproate, lamotrigine, carbamazepine, topiramate and phenytoin

Answer 32

prognosis - dependant on cause | complications - death, paralysis

Answer 33

* Serious inflammation of the meninges caused by various bacteria e.g. strep pneumoniae, Neisseria menigitidis and H. influenzae type b are the predominant causative pathogens in both adults and children * Meningitis resulting from infection with Neisseria Meningitides is known as meningococcal disease * Meningitis resulting from infection with Streptococcus pneumoniae is known as pneumococcal disease. * In neonates (younger than one month of age), Streptococcus agalactia, Escherichia coli, S. pneumoniae, and Listeria monocytogenes are the most common causative organisms

Answer 34

incidence 2-5 per 100,000 | can affect adults and children

Answer 35

* Bacteria reach the CNS either by haematogenous spread (the most common route) or by direct extension form a contigious site * Neonates can acuire pathogens from non-sterile maternal genital secretions through the placent or from their surroundings * Bacteria multiply quickly once they have entered the subarachnoid spae * Bacterial components in the cerebrospinal fluid incude the production of various inflammatory mediators, which in turn enhance the influx of leukocytes into the CSF * Inflammatory cascade leads to cerebral oedema and increase ICP which contribute to neurological damage and even death

Answer 36

* Under 5 or over 65 * Crowding * Exposure to pathogens * Non-immunised infants * Immunodeficiency * Cancer * Asplenia/hyposplenic state * Cranial anatomical defects * Cochlear implants

Answer 37

* Presence of risk factors * Headache * Neck stiffness – stiff neck with resistance to passive neck flexion (nuchal rigidity) * Fever * Altered mental status – in older pts this may be the only presenting sign of meningitis * Confusion – in older pts this may be the only presenting sign of meningitis * Photophobia * Vomiting * Seizures * Infants: hypothermia, irritability, lethargy, poor feeing, apnoea

Answer 38

* Kerning’s sign: patient is uspine and the thigh flexed to a 90 right angle, attempts to straighten or extend the leg are met with resistance * Brudzinski’s sign: flexion of the neck causes involuntary flexion of knees and hips * Non-blanching rash

Answer 39

* Encephalitis * Viral meningitis * Drug-induced meningitis * TB meningitis * Fungal meningitis

Answer 40

- CSF CELL COUNT AND DIFFERENTIAL: polymorphonuclear pleocytosis - CSF PROTEIN: elevated - CSF GLUCOSE: low - CSF GRAM STAIN: positive - CSF CULTURE: positive - ANTIGEN DETECTION IN CSF: Neisseria meningitides capsular polysaccharide antigen - BLOOD CULTURE: positive - FBC AND DIFFERENTIAL: leucocytosis, anaemia, thrombocytopenia

Answer 41

• 1st LINE: - ADMIT THE PT TO HOSPITAL AS AN EMERGENCY BY TELEPHONING 999 - WITH BLANCHING RASH  EMPIRIC Abx: give benzylpenicillin IV, give IM if a vein is not available (inject as proximally as possible preferably into a part of the limb that is still warm as cold areas will be less well perfused) - WITHOUT NON-BLANCHING RASH: all people should be transferred directly to secondary care without giving parenteral abx unless urgent transger to hospital is not possible, if this is the case parenteral abx should be administered in primary care  ampicillin

Answer 42

prognosis - with tx, good outcome | complications - shock, elevated ICP, hydrocephalus, seizures, hearing loss

Answer 43

• Inflammation of the meninges caused by a vairtey of different viruses and is the most common cause of aseptic meningitis

Answer 44

* Enteroviruses are spread by the faecal-oral route * Non-polio enteroviruses and arboviruses initially replicate outside the CNS in tissues such as muscle, liver, and the respiratory or GI tacts and then reach the cns by haematogenous spread * Viral penetration fo the blood-brain barrier occurs by either infection of endothelial cells or of migrating leukocytes * Once within the CNS, viruses spread through the subarachnoid space leading to meningitis and may go on to infect neurons and glial cells leading to encephalitis or myelitis * Cellular ummune response to viral infection of the CNS leads to the accumulation of lymphocytes within the CSF and the release of inflammatory cytokines such as IL-6 and tnf * The inflammatory response increases the permeability of the blood-brain barrier and this allows diffusion of circulating immunoglobulins into the CSF

Answer 45

incidence of 2-5 per 100,000 | adults and children

Answer 46

* Infants and young children * Young adults * Older people * Summer and autumn * Exposure to mosquito or tick vector * Unvaccinated for mumps

Answer 47

* Presence of risk factors * Headache * Nausea and vomiting * Photophobia * Neck stiffness * Fever

Answer 48

* Non-blanching rash * Kerning’s sign: patient is uspine and the thigh flexed to a 90 right angle, attempts to straighten or extend the leg are met with resistance * Brudzinski’s sign: flexion of the neck causes involuntary flexion of knees and hips

Answer 49

* Encephalitis * Meningitis, bacterial * Drug-induced meningitis * TB meningitis * Cryptococcal meningitis

Answer 50

• 1ST LINE: - CSF MICROSCOPY: WBC >5 cells/mm^3 for children and adults and >20 cells/mm^3 for neonates - CSF GRAM STAIN: negative in viral, positive in bacterial - CSF BACTERIAL CULTURE: negative - CSF PROTEIN: normal or elevated - CSF GLUCOSE: may be low - CT/MRI HEAD SCAN: unremarkable, may exclude abscess or bacterial meningitis

Answer 51

• 1st LINE: - SUPPORTIVE CARE: adequate hydration, use of antipyretics for fever, anti-emetics if vomiting and analgesia for headaches

Answer 52

prognosis - generally very good | complications - persistent headache and malaise, neuro-developmental deficits in infants

Answer 53

* Migraine is a chronic, genetically determined, episodic neurological that usually presents in early-to-mid life * Pts complain of intermittent headache and associated symptoms such as visual disturbance, nausea, vomiting and sensitivity to light or noise (photophobia and phonophobia)

Answer 54

• Prevalence: 18%, mean age of onset 18years. Men 6% with mean age of onset 14 years. mainly adults

Answer 55

* Headache of migraine results from neurogenic inflammation of first-division trigeminal sensory neurons that innervate the large vessels and meninges of the brain * Causes a change in the way that pain is processed by the brain * Increased neuronal activity can be demonstrated in areas of the brainstem during migraine, and this persists even when the headache is relieved by triptans * It is not known whether this brainstem activation reflects the cause of migraine (the so called brainstem generator) or instead signifies activation of endogenous pai-control systems * When activated, the trigeminal neurons release substances that cause dilation of mnenigeal blood vessels, leakage of plasma proteins into surrounding tissue and platelet actovation * This sensitises nerve fibres so that previously ignored stimuli such as the normal pulsations of meningeal vessels are interpreted as painful

Answer 56

* Fx of migraine * High caffeine intake * Exposure to change in barometric pressure * Female * Obesity * Habitual snoring * Stressful life events * Overuse of headache medications * Lack of sleep

Answer 57

* Prolonged headache – a headache that lasts 4-72 hours if untreated is suggestive of migraine * Nausea – ‘sick headache’ * Decreased ability to function * Headache worse with activity * Sensitivity to light

Answer 58

* Tension headache * Cluster headache * PTSD * SAH * Cerebral neoplasm

Answer 59

• 1st LINE: - CLINICAL DIAGNOSIS: diagnosis is based on Hx and physical exam, testing is not used to ‘rule in’ diagnosis of migraine but rather ‘rule out’ plausible alternative diagnoses that are suggested by the pts presentation  FULFILS ICH-IIb CRITERIA FOR MIGRAINE

Answer 60

• 1st LINE: - MILD-TO-MODERATE NSAID/ASPIRIN: aspirin or ibuprofen, pts with nausea + metoclopramide (anti-emetic)  metoclopramide should not be used regularly due to the risk of extrapyramidal side effects - SEVERE: triptan e.g. almotriptan, if pt has aura triptans should be taken at the start of the headache and not at the start of the aura - If pregnant give paracetamol instead of NSAID/ASPIRIN

Answer 61

prognosis - do well with treatment | complications - depression, chronic migraine, migrainous infection

Answer 62

* Tension-type headaches can be either episodic or chronic * They are rarely disabling or associated disabling or associated with significant autonomic phenonmena, thus patients do not usuallt seek medical care and usually sucessfullt self-treated * Pain is typically expressed as being a ‘tight’ band around the head * It does not worsen with routine physical activity

Answer 63

* Lifetime risk 70-80% (very surprised it’s not higher) * About 50% of adults aged 40 years’ experience episodic tension-type headaches * The prevalence is higher in woman then men

Answer 64

* Muscle contraction is often considered the cause of pain in tension-type headaches, but there is little evidence to support this * In tension-type headaches, perifranial muscle vontraction is normal or slightly increased and the extent of muscle contraction does not correlate with the extent of head pain * Psychological stress is the most common trigger for tension-type headache * Extended periods of mental tension or psychological stress may play a role in central desensitisation and the development of chronic tension-type headache * Disturbed sleep patterns can trigger an episodic tension-type headache * Insomnia and other sleep disorders associated with chronic tension-type headache

Answer 65

* Mental tension * Stress * Missing meals * Fatigue

Answer 66

* Presence of riskf actors * Generalised head pain – bilateral pressure like, non-throbbing pain * Frontal or occipital head pain * Non-pulsatile dull head pain * Constricting pain – pain expressed as tight band around head * Normal neurological examination – abnormal should prompt investigation for possible causes of secondary headaches

Answer 67

* No photophobia or phonophobia | * Neck muscle tenderness

Answer 68

* Chronic migraine * Medicine overuse headache * Sphenoid sinusitis * Giant cell arteritis * Temporomandibular disorder * Pituitary tumour/brain tumour * Chronic subdural haematoma

Answer 69

• 1ST LINE: - CLINICAL DIAGNOSIS: imaging and lab studies do not aid in the diagnosis of tension-tyoe ehadaches and should only be considered in refractory or progressive cases  typical headache without associated features (nausea, vomitnh), normal neurological exam

Answer 70

• 1st LINE: - ACUTE: paracetamol/NSAIDs e.g. ibuprofen/naproxen - CHRONIC: antidepressants e.g. amitriptyline

Answer 71

prognosis - self tx with simple analgesic medicine is usually effective complications - peptic ulcer

Answer 72

* Chronic progressive neurological disorder characterised by motor symptoms * Parkinsonism is an umbrella term for the clinical syndrome involving bradykinesia together with at least one of the following: rigidity, tremor and postural instability * Parkinson’s disease is the most common form of parkinsonism * Other causes include: drug induced, CVD, lewy-body dementia, multiple system atrophy, and progressive supranuclear palsy * With parkinsons disease, there is a progressive depletion of dpomaine-secreting cells in the substantia nigra but th actual cause is unknown

Answer 73

* Prevalence: 120-230 per 100,000 (0.12-0.23%) * 1% of people older than 65 are diagnosed with it * 4-8% of people with Parkinson’s are below 50. 1.5X more common in men.

Answer 74

* Selective loss of nigrostriatal dopaminergic neurons in the substania nigra pars compacta occurs with findings of intracytoplasmic eosinophilic inclusions and neurites both of which are composed of the protein synuclein * Loss of striatal dopaminergic output within the circuitry of the basal ganglia accounts for the constellation of motor symptoms * Bradykinesia correlates with dopamine feficient with reduced striatal fluorodopa uptake, results in excessive stimulation of the subthalamic nucleus and the GPi which results in slowness and delay initiating movement = symptoms including loss of dexterity, drooling, monotonous voice, loss of facial expression and reduced arm swing

Answer 75

* Increasing age * Hx of familial PD in younger-onset disease * Mutation in gene encoding glucocerebrosidase (GBA) * 1-methyl-4-phenul-1,2,3,6,-tetrahydropyridine (MPTP) exposure – neurotoxin

Answer 76

* Presence of risk factors * Bradykinesia – slowness of movements, progressive reduction in amplitude of repeated movements, delay in initiating movements and freezing of gait are eventually seen in all pts * Resting tremor – onset is asymmetrical, chin tremor may occur, tremor may re-emerge when the arms are outstretched * Rigidity – hypertonicity is defined as unvarying increased resistance within the range of passive movement about a joint * Postural instability – imabalance or falling noted with pull test or spontaneously; retropulsion, common in mild-to-late stage disease

Answer 77

* Progressive supranuclear palsy * Lewy body dementia * Coritcobasal degeneration * Alzheimer’s disease with parkinsonism

Answer 78

• 1ST LINE: - DOPAMINERGIC AGENT TRIAL: diagnosis of PD is made clinically and in cases without atypical features no additional diagnostic testing is indicated, if diagnostic testing is warranted due to atypical features or unclear clinical diagnosis, tests may include dopaminergic agent trial  improvement in symptoms

Answer 79

• 1ST LINE: - LEVODOPA: dopa carboxylase inhibitor (co-beneldopa or co-careldopa), usually offered to people in the early stages of parkinson’s disease who motor symtpoms impact on their QOL • 2ND LINE: - ORAL MONOAMINE OXIDASE-B INHIBITORS: selegiline, rasagiline, or safinamide OR - AMANTADINE

Answer 80

prognosis - no cure, about symptom management, course is progressive with rates of progression varying from pt to pt complications - • Levodopa-induced dyskinesias, motor fluctuations, dementia, constipation

Answer 81

• Inflammatory demyelinating disease characterised by the presence of episodic neurological dysfunction in at least two areas of the CNS (brain, spinal cord and optic nerves) separated in time and space

Answer 82

most common cause of neurological disability among young adults F:M 3:1

Answer 83

• INFLAMMATION: - Lymphocytes with encephalitogenic potential are activated in the periphery by factors such as infection or other metabolic stress - These activated t cells seek entry into the CNS via attachment to a receptor on endothelial cells - This interaction, mediated by production of matrix metalloproteinases, allows a breach in the blood-brain barrier leading to further upregulation of endothelial adhesion molecules and additional influx of inflammatory cells - The T cells produce inflamamotry cytokines that cause direct toxicity also attract macrophages that contribute to demyelination - Epitope spread occurs early and contributes to the complexity of the immunopathology • DEGENERATION: - Believed to reflect axonal degeneration and loss - Demyelination disrupts axonal support and leads to destabilisation of axonal membrane potentials, which causes distal and retrograde degeneration over time - There is also a suggestion that inflammatory cells, abs, and complement may contribute to axonal injury - Axonal damage has been identified in regions of active inflammation, indicating that it begins early in the disease process • Pathologically, MS is characterised by multifocal areas of demyelination, loss of oligodendrocytes, and astrogliosis with loss of axons primarily in the white matter of the CNS, although cortical lesions may also play a significant role

Answer 84

* Female * Northern laititude * Genetic factors * Smoking * Vit d deficiency

Answer 85

* VISUAL DISTURBANCE IN ONE EYE: grayin or blurring of vision in one eye (can be described as looking through pertroleum jelly), may have pain in moving that eye and describe loss of colour discrimination, particularly reds * ABNORMAL EYE MOVEMENTS: nystagmus may be present * PECULIAR SENSORY PHENOMENA: pts often describe odd sensations of a patch of wetness or burning, or hemibody sensory loss or tingly, in particular banding or hemibanding is associated with spinal cord lesions * LHERMITTE’S SIGN: electric shcok-like sensations extending down the cervical spine radiating to the limbs * Trigeminal neuropathy or neuralgia * FOOT DRAGGING: pts will often describe gradual onset of weakness after walkig several streets or several miles such that the foot slaps the ground – this weakness resolves with rest * LEG CRAMPING: involuntary movement in the lower leg with cramping or jerking in the calves, particularly at night or while driving * BOWEL DYSFUNCTION: constipation is commonly seen in MS * URINARY FREQUENCY: multifactorial causes including damage to the cns resulting in urinary retention and detrusor instability, UTIs are more frequent in pts with urinary retention

Answer 86

* Myelopathy due to cervical spondylosis * Fibromyalgia * Sleep disorders * Vit B12 deficiency

Answer 87

• 1st LINE: - MRI – BRAIN: hyperintensities in the periventricular white matter, most sensitive images are sagittal FLAIR - MRI – SPINAL CORD: demyelinating lesions in the spinal cord, particularly the cervical spinal cord, detection of alternate diagnosis such as cervical spondylosis - FBC: should be normal - COMPREHENSIVE METABOLIC PANEL: should be normal - TSH: normal - VIT B12: normal

Answer 88

• 1ST LINE: | - CORTICOSTEROIDS: 3-day high dose of methylprednisolone

Answer 89

prognosis is difficult to say | complications include UTIs, osteoporosis, depression, visual impairment, erectile dysfunction

Answer 90

neurological problem which presents as symmetrical weakness of proximal upper and/or lower limbs

Answer 91

relatively uncommon disease

Answer 92

* PRIMARY: muscular dystrophy (disorders of dystrophin) e.g. Duchenne muscular dystrophy, congenital myopathies (centronuclear myopathy), metabolic myopathies (lipid storage disease) * ACQUIRED: secondary metabolic and endocrine myopathies thyroid diseases, parathyroid dysfunction, pituitary dysfunction, corticosteroids, biochemical and DM

Answer 93

* Female * Older * Hypertension * Untreated hypothyrodisim * Rnela or hepatic disease

Answer 94

* Weakness predominantly affecting proximal muscle groups (shoulder and limb girdles) is typical * Weakness manifests itself in different ways at different ages * Reduced muscle strength and power in older children and adults * Myalgia may occur in inflammatory myopathies * Muscle-strength reflexes are preserved * Somatosensory reflexes are preserved * Muscle tone normal or reduced * Symmetrical proximal muscle weakness * Malaise * Fatigue * Absence of sensory symptoms (paraesthesia) * Atrophy of msucles (and reduced reflexes) occurs late with myopathies (early with neuropathy)

Answer 95

* Guillain-Barre syndrome * Lambert-Eaton myasthenic syndrome * Myasthenia gravis * Cerebral palsy * Spinal muscular atrophy

Answer 96

• 1st LINE: - FBC - URINALYSIS - ECG: may show changes of hypokalaemia, increase P-R interval, U waves, wide QRS and non-specific ST-T changes, sinus arrhythmias, deep Q waves and elevated R waves precordially - CK - U&E’s - SERUM MYOGLOBIN - ESR - ANTINUCLEAR Abs - ELECTROMYOGRAPHY: excludes primarily neurogenic processes, proximal muscles of lower extremities often exhibit the most prominent features, often helps to confirm diagnosis but is not in itself diagnostic

Answer 97

• 1ST LINE: - MYOPATHY ASSOCIATED WITH RESPIRATORY FAILURE: monitor pulmonary function (early restrictive pattern may occur before onset of symptoms), beware of symptoms of nocturnal hypoxia (poor sleep, nightmares, headaches), physio, may require permanent ventilation - SPECIFIC MEDICATION MAY BE USEFUL IN PARTICULAR SITUATIONS - SURGERY: tendon release surgery to prolong ability to walk

Answer 98

prognosis is dependant on the specific diagnosis complications include respiratory failure, aspiration pneumonia, MSK problems