Neurology Flashcards

Question

what environmental factors may lead to epilepsy?

Answer 1

Prenatal and perinatal risk factors - maternal drug use, infection during pregnancy, preterm birth, low birth weight, neonatal seizures, Hypoxic ischaemic encephalopathy CNS infections Cerebrovascular disease - e.g. stroke Traumatic brain injury Brain tumours Mixed genetic and environmental - neurocutaneous syndromes - conditions such as tuberous sclerosis complex, neurofibromatosis type 1 and Struge weber syndrome have genetic and environmental tigers

Answer 2

Focal Onset Seizure Generalised onset seizure Unknown onset seizure

Answer 3

Focal aware seizure (previously simple partial seizures) - individual remains conscious and can recall events during the seizure. Focal Impaired awareness seizure (previously complex partial seizure) - involves alteration in consciousness - they may start as focal aware seizures and then progress Focal to Bilateral Tonic-Clonic Seizures: Begin in one hemisphere and spread to involve both, resulting in a tonic-clonic seizure.

Answer 4

These arise at some point within, and rapidly engage, bilaterally distributed networks. Tonic-Clonic Seizures: Characterised by stiffening (tonic phase) followed by rhythmic muscle jerking (clonic phase). Absence Seizures: Brief lapses in consciousness, often with staring. They can be sub-classified into typical and atypical absence seizures. Tonic Seizures: Cause stiffening. Atonic Seizures: Lead to loss of muscle control, often resulting in falls ('drop attacks'). Clonic Seizures: Involves repetitive jerking movements. Myoclonic Seizures: Quick, sudden jerks of a muscle or group of muscles.

Answer 5

Childhood Absence Epilepsy (CAE): Characterised by typical absence seizures, with onset usually between 4-10 years. Juvenile Myoclonic Epilepsy (JME): Marked by myoclonic jerks, typically shortly after waking. Dravet Syndrome: Severe epilepsy beginning in infancy, initially presenting as prolonged seizures with fever. Lennox-Gastaut Syndrome: Characterised by multiple seizure types, cognitive dysfunction, and a specific EEG pattern.

Answer 6

Bloods - FBC, Electrolytes, glucose, LFTs U&E's EEG - electoencephalogram MRI LP, Genetic testing, prolonged EEG monitoring

Answer 7

Syncope Psychogenic non-epileptic seizures TIA Alcohol withdrawal seizure Seizures secondary to metabolic/toxic disturbance

Answer 8

Normally start anti-epileptics after a second seizure Sodium valproate is considered the first line treatment for patients with generalised seizures with carbamazepine used for focal seizures. Generalised tonic-clonic seizures sodium valproate second line: lamotrigine, carbamazepine Absence seizures* (Petit mal) sodium valproate or ethosuximide sodium valproate particularly effective if co-existent tonic-clonic seizures in primary generalised epilepsy Myoclonic seizures** sodium valproate second line: clonazepam, lamotrigine Focal seizures carbamazepine or lamotrigine second line: levetiracetam, oxcarbazepine or sodium valproate *carbamazepine may exacerbate absence seizures **carbamazepine may exacerbate myoclonic seizures

Answer 9

Can't drive for 6 months following a seizure. If patients have established epilepsy then they must be seizure free for 12 months.

Answer 10

the patient has a neurological deficit brain imaging shows a structural abnormality the EEG shows unequivocal epileptic activity the patient or their family or carers consider the risk of having a further seizure unacceptable

Answer 11

For people having a tonic-clonic seizure lasting more than 5 minutes, or who have more than three seizures in an hour - Buccal midazolam as first-line treatment in the community. Rectal diazepam if preferred, or if buccal midazolam is not available. Intravenous lorazepam if intravenous access is already established and resuscitation facilities are available.

Answer 12

Dysdiadochokinesia & Dysmetria (past pointing) Inability to perform and sustain a series of rapidly alternating muscle movements. The patient overshoots when attempting to reach a point with their finger Ataxia Gross incoordination of muscle movements. The patient may be very unsteady on their feet towards the side of the lesion. The patient may also show rebound, where pushing down on the outstretched upper limb causes it to rebound up past its original position Nystagmus A repetitive, involuntary oscillation of the eyes. The patient may also complain of blurred vision Intention tremor A wide tremor during voluntary movements, such as holding out the hands Slurred speech Speech may be imprecise, slow and distorted Hypotonia The patient may have muscle weakness on the side of the lesion

Answer 13

The focus on management in hyperacute stroke units and the specialist services they offer (i.e. thrombolysis and thrombectomy) Understanding that not every hospital has a hyperacute stroke unit - and hence knowing where and how to refer in the event of a suspected stroke The existence of specialist and dedicated acute stroke teams in hospitals - including consultants, registrars and specialist nurses, enabling rapid responses and immediate specialist expertise for suspected strokes “Time is brain” - investigations should not delay transfer to hyperacute stroke units

Answer 14

chronic autoimmune neuromuscular disease The hallmark of the condition is muscle weakness that increases during periods of activity and improves after rest. It primarily affects the ocular muscles, leading to ptosis and diplopia, but can also involve bulbar, limb and respiratory muscles.

Answer 15

postsynaptic nicotinic acetylcholine receptors (AChRs) at the neuromuscular junction, impairing neuromuscular transmission. Other patients may have antibodies against muscle-specific kinase (MuSK)

Answer 16

Genetic predisposition - HLA-B8, DR3 haplotype has been associated with early onset MG, HLA b27/ DR15/16 linked to late onset Environmental triggers - certain infections can trigger an autoimmune response leading to MG. - Thymoma is found in 10-15% of patients - these tumours can induce an immune response resulting in the productive of autoantibodies against acetylcholine receptors Hormonal influnces

Answer 17

autoantibodies against components of the neuromuscular junction (NMJ), particularly the nicotinic acetylcholine receptor (nAChR). = reduction in the number and functionality of nAChRs at the postsynaptic membrane, thereby disrupting neurotransmission at the NMJ. The diminished nAChR density leads to a decreased safety factor for neuromuscular transmission, which manifests as muscle weakness in patients with MG. Also AB against muscle specific kinase and lipoprotein-related protein 4 (LRP4) - both essential for proper NMJ formation and maintenance. The presence of these autoantibodies and their respective pathogenic mechanisms contribute to the heterogeneity observed in MG clinical presentation.

Answer 18

The hallmark of MG is fluctuating muscle weakness that worsens with repetitive activity and improves with rest. ptosis (drooping of the upper eyelid), diplopia (double vision), dysarthria (difficulty speaking), dysphagia (difficulty swallowing), and proximal limb weakness. Myasthenic crisis - respiratory involvement - life threatening

Answer 19

penicillamine quinidine, procainamide beta-blockers lithium phenytoin antibiotics: gentamicin, macrolides, quinolones, tetracyclines

Answer 20

Repetitive nerve stimulation Single-fiber electromyography (most sensitive test) Anti-acetylcholine receptor (AChR) antibodies Anti-muscle-specific kinase (MuSK) antibodies Anti-lipoprotein-related protein 4 (LRP4) antibodies CT chest or MRI - to assess for thymoma or thymic hyperplasia

Answer 21

Lambert-Eaton Syndrome (autoimmune disorder affecting the neuromuscular junction. However, it primarily affects voltage-gated calcium channels at the presynaptic nerve terminal). LES typically presents with proximal muscle weakness that improves with repeated use (unlike MG where symptoms worsen with use). - Commonly get dry mouth. GBS - GBS is an immune-mediated polyradiculoneuropathy characterised by rapidly progressive bilateral limb weakness and loss of tendon reflexes. GBS often presents with ascending paralysis starting from the lower extremities. Sensory disturbances may also be present. The progression of symptoms in GBS is usually over days to weeks, whereas in MG it is more variable and often fluctuates during the day. Pupillary responses remain intact in GBS unlike in some cases of MG where pupillary involvement can occur due to cranial nerve involvement. Botulism - a neurotoxic disorder caused by Clostridium botulinum that blocks acetylcholine release at the neuromuscular junction. Unlike MG, botulism often presents with a descending paralysis starting from cranial nerves, leading to symptoms such as diplopia and dysphagia. Autonomic symptoms including dry mouth, constipation and urinary retention are common in botulism but rare in MG. In contrast to MG, muscle weakness in botulism does not improve with rest or anticholinesterase medications.

Answer 22

Acetylcholinesterase inhibitors such as pyridostigmine. If symptoms persist - consider immunosuppressive agents - Steroids are often first line - other options = azathiorprine, mycophenolate mofetil, cyclosporine. IVIG or plasma exchange may be consider in severe cases or during myasthenia crisis Surgical - thymectomy

Answer 23

abdominal cramps, diarrhoea and excessive salivation

Answer 24

n a myasthenic crisis, immediate hospitalisation is required. Intensive respiratory support may be necessary, including intubation and mechanical ventilation if there is impending respiratory failure. Rapid short-term symptom control can be achieved by plasma exchange or IVIg.

Answer 25

acute polyradiculoneuropathy characterised by rapidly evolving ascending muscle weakness with mild sensory changes Autoimmune Precipitated by infection - most common Campylobacter, EBV, CMV Occasionally vaccines have been associated with it Some studies suggest an increased risk of GBS following surgical procedures

Answer 26

cross reaction of antibodies with gangliosides in the peripheral nervous system correlation between anti-ganglioside antibody (e.g. anti-GM1) and clinical features has been demonstrated anti-GM1 antibodies in 25% of patients

Answer 27

progressive weakness of all four limbs Weakness is classically ascending i.e in the lower extremities there may be a history of gastroenteritis areflexia cranial nerve involvement e.g. diplopia autonomic involvement: e.g. urinary retention, diarrhoea

Answer 28

LP - rise in protein with a normal white blood cell count (albuminocytologic dissociation) found in 66% Nerve conduction studies may be performed

Answer 29

variant of Guillain-Barre syndrome associated with ophthalmoplegia, areflexia and ataxia. The eye muscles are typically affected first usually presents as a descending paralysis rather than ascending as seen in other forms of Guillain-Barre syndrome anti-GQ1b antibodies are present in 90% of cases

Answer 30

- acute transverse myelitis (ATM) - apid onset of spinal cord dysfunction, which may mimic the ascending weakness seen in GBS. Key distinguishing features include: Sensory level: A clear sensory level is indicative of ATM and not typically seen in GBS. Bladder or bowel dysfunction: More commonly associated with ATM than GBS at onset. MRI findings: In ATM, T2-weighted images often show hyperintense lesions in the spinal cord. - Chronic Inflammatory demyelinating polyneuropathy - similar to GBS - important differences: Course of disease: CIDP has a more protracted course, developing over at least two months, while GBS typically presents acutely over days to weeks. Response to treatment: CIDP patients usually respond well to immunosuppressive therapy and may require long-term treatment; whereas GBS is generally self-limiting once treated. Botulism - can resemble but differences are - Eyelid ptosis and fixed pupils: These are early signs in Clostridium botulinum poisoning but are not common in GBS. History of food ingestion: A history of ingestion of home-canned, preserved or fermented foods can point towards botulism. Descending paralysis: Botulism typically presents with a descending pattern of weakness, whereas GBS is classically ascending.

Answer 31

plasma exchange IV immunoglobulins (IVIG): as effective as plasma exchange. No benefit in combining both treatments. IVIG may be easier to administer and tends to have fewer side-effects steroids and immunosuppressants have not been shown to be beneficial FVC regularly to monitor respiratory function

Answer 32

Respiratory complications (mechanical ventilation is required in 30% of patients) Autonomic dysregulation (labile BP, arrhythmias, cardiac arrest due to involvement of autonomic fibres) DVT Muscle atrophy Contractures pressure sores Persistent numbers, tingling or pain in the limbs

Answer 33

age > 40 years poor upper extremity muscle strength previous history of a diarrhoeal illness (specifically Campylobacter jejuni) high anti-GM1 antibody titre need for ventilatory support

Answer 34

Bell's palsy is an acute neurological condition presenting with rapid onset of unilateral facial paralysis. The exact cause is unknown but it has been linked to the herpes simplex virus.

Answer 35

Pregnancy Severe pre-eclampsia Hypertension Obesity Diabetes mellitus Upper respiratory tract infections

Answer 36

unilateral facial paralysis acute onset - 72 hours the inability to wrinkle forehead and close eye fully on the affected side oss of the nasolabial labial fold, and drooping of the mouth, which is more pronounced when the patient tries to smile Pain in the ear and surrounding area loss of taste in the anterior tongue Hyperacusis (increases sensitivity to noise **forehead sparing suggests an upper motor neurone cause

Answer 37

Stoke or TIA Brain tumour Ramsey Hunt - reactivation of VZV which can cause unilateral facial paralysis but typically also has painful vesicular rash

Answer 38

Good eye care - artificial eye drops, use tape overnight, wearing sunglasses Support nutrition with straws and soft diet Prednisoolone if present within 72 hours of onset Antivirals Ensure follow up appointment to monitor recovery

Answer 39

Synkinesis: This is characterised by involuntary muscular movements accompanying voluntary movements. It occurs due to aberrant regeneration of the facial nerve and may present as crocodile tears syndrome (lacrimation during eating), gustatory sweating or hemifacial spasm. Persistent facial weakness Corneal keratitis Lagophthalmos Abrasive keratopathy

Answer 40

Most patients can expect to see signs of recovery within 3 weeks and complete recovery within 4 months.

Answer 41

a rare, life-threatening condition triggered by neuroleptic or antipsychotic medication a neurological emergency characterised by hyperthermia, altered mental status, muscle rigidity and autonomic dysregulation

Answer 42

ntipsychotics: Both typical (e.g., haloperidol) and atypical (e.g., risperidone) antipsychotics are primary offenders. Other Medications: Antiemetics like metoclopramide, which have dopamine-blocking effects, may also trigger the syndrome.

Answer 43

It occurs within hours to days of starting an antipsychotic (antipsychotics are also known as neuroleptics, hence the name) and the typical features are: - pyrexia - muscle rigidity - autonomic lability: typical features include hypertension, tachycardia and tachypnoea - agitated delirium with confusion

Answer 44

- primarily a clinical diagnosis based on the presence of cardinal symptoms: hyperthermia, autonomic dysregulation, altered mental status, and lead-pipe rigidity. Bloods Leukocytosis is commonly seen in NMS May have elevated CK levels If suspicion of neuroinflammatory condition which might mimic NMS - may need LP to exclude this CT or MRI to exclude space occupying lesion

Answer 45

stop offending agent ICU admission Hydrations and electrolyte management Treatment of hyperthermia Dopamine agonists if symptoms persist despite supportive care, considering dopamine agonists like bromocriptine and amantaide Dantrolene can be considered in severe cases resistant to other treatments

Answer 46

Cardiovascular complications: These are amongst the most serious and frequent complications. They include arrhythmias, hypotension, myocardial infarction and cardiac arrest. Pulmonary complications: Acute respiratory distress syndrome (ARDS), aspiration pneumonia, pulmonary oedema and respiratory failure may occur due to dysphagia and altered consciousness. Renal complications: Acute kidney injury is a common complication of NMS. It is typically caused by rhabdomyolysis leading to myoglobinuria. Musculoskeletal complications: Severe muscle rigidity can lead to rhabdomyolysis which can further cause renal impairment or failure. Hepatic complications: Hepatotoxicity or liver dysfunction may occur due to drug-induced liver injury or secondary to systemic inflammatory response syndrome (SIRS).

Answer 47

monoamine oxidase inhibitors SSRIs St John's Wort, often taken over the counter for depression, can interact with SSRIs to cause serotonin syndrome tramadol may also interact with SSRIs ecstasy amphetamines

Answer 48

neuromuscular excitation hyperreflexia myoclonus rigidity autonomic nervous system excitation hyperthermia sweating altered mental state confusion

Answer 49

supportive including IV fluids benzodiazepines more severe cases are managed using serotonin antagonists such as cyproheptadine and chlorpromazine

Answer 50

Multiple sclerosis (MS) is an inflammatory demyelinating disease, clinically defined by two episodes of neurological dysfunction (brain, spinal cord or optic nerves) separated in space and time.

Answer 51

Vision Problems (optic neuritis - temporary vision loss , scotoma, colour blindness and painful eye movement, pale optic disc on fundoscopy. Fatigue Rain and altered sensation - trinomial neuralgia, chest tightness, Lhermitte's phenomenon (shock like sensation radiating dow the spine induced by neck flexion) Muscle spasticity, stiffness and weakness Mobility issues bladder and bowel dysfunction Sexual dysfunction Depression and enxiety Cognitive impairment Speech and swallowing issues

Answer 52

Usual bloods to rule out alternatives MRI brain MRI brain CSF examination if MRI is not diagnostic

Answer 53

Acute relapse -High dose steroids Disease modifying drugs Typical indications for disease-modifying drugs include: relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaided secondary progressive disease + 2 relapses in past 2 years + able to walk 10m (aided or unaided) Options Natalizumab Ocrelizumab fingolimod Trial of amantadine for fatigue Baclofen and gabapentin for spasticity

Answer 54

meningitis encephalitis subarachnoid haemorrhage head injury sinusitis glaucoma (acute closed-angle) tropical illness e.g. Malaria

Answer 55

Typically patient > 60 years old Usually rapid onset (e.g. < 1 month) of unilateral headache Jaw claudication (65%) Tender, palpable temporal artery Raised ESR

Answer 56

Neisseria meningitidis, Streptococcus pneumoniae, or Haemophilus influenzae.

Answer 57

Classic Triad - fever - Neck stiffness (Nuchal rigidity) - altered mental state Malaise, headache, myalgia, Kernig's sign: In a supine patient with hips and knees flexed at 90 degrees, pain on straightening the knee suggests meningeal irritation. Brudzinski's sign: Passive flexion of one hip leading to involuntary flexion of the other hip is another indicator of meningeal irritation.

Answer 58

Blood cultures FBC CRP and ESR Blood glucose LP - microscopy and gram stain - culture - PCR - CSF glucose and protein

Answer 59

Encephalitis - focal neurological signs such as hemiparesis or aphasia are more common in encephalitis. In contrast to the nuchal rigidity frequently seen in meningitis, this is less commonly observed in encephalitis. The presence of seizures at onset is more suggestive of encephalitis than meningitis. SAH Brain Abscess - Focal neurological deficits are common in brain abscess and less so in meningitis. Brain abscess often has a more gradual onset of symptoms over days to weeks, while meningitis typically presents acutely.

Answer 60

Empirical therapy with 3rd generation cephalosporin (ceftriaxone or cefotaxime) plus ampicillin Add acyclovir

Answer 61

hearing loss Cognitive impairment seizures Sepsis Waterhouse-friderichsen syndrome - This is a severe complication of Neisseria meningitidis infection characterised by adrenal gland failure due to haemorrhage, leading to shock and disseminated intravascular coagulation (DIC). Visual loss Subdural effusions and empyemas Cerebral abscesses

Answer 62

Vasovagal syncope: This is the most common cause of syncope and occurs due to a sudden drop in blood pressure and heart rate. It is often triggered by emotional stress, pain, or standing for long periods. Cardiac syncope: This type of syncope occurs due to a problem with the heart's electrical system, such as an arrhythmia or heart block. It is more common in older adults and those with a history of heart disease. Orthostatic hypotension: This is a sudden drop in blood pressure that occurs when a person stands up from a sitting or lying position. It can be caused by dehydration, medication side effects, or underlying medical conditions. Neurological syncope: This type of syncope occurs due to a problem with the brain or nervous system, such as a seizure disorder or stroke. It is less common than the other types of syncope but should be considered in patients with a history of neurological conditions. Hypoglycemia: Low blood sugar levels can cause syncope, especially in patients with diabetes who take insulin or other medications that lower blood sugar levels. It is less common than the other types of syncope but should be considered in patients with a history of diabetes or other metabolic disorders.

Answer 63

Situational syncope: This occurs during specific situations like micturition, defecation or coughing. The pathophysiology involves an abrupt drop in blood pressure due to a strong vagal response.

Answer 64

Carotid sinus hypersensitivity: It's characterised by an exaggerated response to carotid sinus baroreceptor stimulation leading to bradycardia and/or vasodilation. It often presents in elderly patients who turn their head or wear tight collars.

Answer 65

Benign paroxysmal positional vertigo (BPPV) is one of the most common causes of vertigo encountered. It is characterised by the sudden onset of dizziness and vertigo triggered by changes in head position. The average age of onset is 55 years and it is less common in younger patients

Answer 66

Features vertigo triggered by change in head position (e.g. rolling over in bed or gazing upwards) may be associated with nausea each episode typically lasts 10-20 seconds positive Dix-Hallpike manoeuvre rapidly lower the patient to the supine position with an extended neck a positive test recreates the symptoms of benign paroxysmal positional vertigo rotatory nystagmus

Answer 67

BPPV has a good prognosis and usually resolves spontaneously after a few weeks to months. Symptomatic relief may be gained by: Epley manoeuvre (successful in around 80% of cases) teaching the patient exercises they can do themselves at home, termed vestibular rehabilitation, for example Brandt-Daroff exercises Medication is often prescribed (e.g. Betahistine) but it tends to be of limited value. Around half of people with BPPV will have a recurrence of symptoms 3-5 years after their diagnosis

Answer 68

Viral labyrinthitis is an inflammatory condition of the inner ear, specifically affecting the labyrinth, which comprises the vestibular system and the cochlea. It is characterized by a sudden onset of vertigo, hearing loss, and tinnitus, typically following a viral infection.

Answer 69

vertigo accompanied by N&V Hearing loss Tinnitus spontaneous unidirectional horizontal nystagmus towards the unaffected side sensorineural hearing loss: shown by Rinne's test and Weber test abnormal head impulse test: signifies an impaired vestibulo-ocular reflex gait disturbance: the patient may fall towards the affected side

Answer 70

episodes are usually self-limiting prochlorperazine or antihistamines may help reduce the sensation of dizziness

Answer 71

Vestibular neuronitis is a cause of vertigo that often develops following a viral infection.

Answer 72

recurrent vertigo attacks lasting hours or days nausea and vomiting may be present horizontal nystagmus is usually present no hearing loss or tinnitus

Answer 73

viral labyrinthitis posterior circulation stroke: the HiNTs exam can be used to distinguish vestibular neuronitis from posterior circulation stroke

Answer 74

buccal or intramuscular prochlorperazine is often used to provide rapid relief for severe cases a short oral course of prochlorperazine, or an antihistamine (cinnarizine, cyclizine, or promethazine) may be used to alleviate less severe cases vestibular rehabilitation exercises are the preferred treatment for patients who experience chronic symptoms

Answer 75

Meniere's disease is a disorder of the inner ear of unknown cause. It is characterised by excessive pressure and progressive dilation of the endolymphatic system.

Answer 76

Age - 20-50 Female family history Underlying causes Viral infections - HSV Allergies Autoimmune disorder vascular factors Genetic factors

Answer 77

recurrent episodes of vertigo, tinnitus and hearing loss (sensorineural). Vertigo is usually the prominent symptom Aural fullness Nystagmus and +ve Romberg test

Answer 78

ENT assessment Inform DVLA Acute attacks - buccal or IM prochlorperazine. Prevention - betahistine and vestibular rehabilitation exercises may be of benefit

Answer 79

HINTS examination - positive HINTS = likely central cause of vertigo Only used in normal full euro exam, persistent vertigo and nystagmus head impulse test, evaluation of nystagmus, and a test of skew.

Answer 80

This test assesses the patient's ability to maintain balance. The patient stands with feet together and eyes closed. A positive test, indicating proprioceptive or vestibular dysfunction, is signalled by swaying or falling.

Answer 81

Trigeminal neuralgia is a pain syndrome characterised by severe unilateral pain. The vast majority of cases are idiopathic but compression of the trigeminal roots by tumours or vascular problems may occur. a unilateral disorder characterised by brief electric shock-like pains, abrupt in onset and termination, limited to one or more divisions of the trigeminal nerve the pain is commonly evoked by light touch, including washing, shaving, smoking, talking, and brushing the teeth (trigger factors), and frequently occurs spontaneously small areas in the nasolabial fold or chin may be particularly susceptible to the precipitation of pain (trigger areas) the pains usually remit for variable periods Management - carbamazepine is first-line failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology

Answer 82

Sensory changes Deafness or other ear problems History of skin or oral lesions that could spread perineurally Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally Optic neuritis A family history of multiple sclerosis Age of onset before 40 years

Answer 83

typically patient > 60 years old usually rapid onset (e.g. < 1 month) headache (found in 85%) jaw claudication (65%) vision testing is a key investigation in all patients anterior ischemic optic neuropathy accounts for the majority of ocular complications. It results from occlusion of the posterior ciliary artery (a branch of the ophthalmic artery) → ischaemia of the optic nerve head. Fundoscopy typically shows a swollen pale disc and blurred margins may result in temporary visual loss - amaurosis fugax permanent visual loss is the most feared complication of temporal arteritis and may develop suddenly diplopia may also result from the involvement of any part of the oculomotor system (e.g. cranial nerves) tender, palpable temporal artery around 50% have features of PMR: aching, morning stiffness in proximal limb muscles (not weakness) also lethargy, depression, low-grade fever, anorexia, night sweats

Answer 84

Temporal arteritis (also known as giant cell arteritis: GCA) is a vasculitis of unknown cause that affects medium and large-sized vessels arteries. It occurs in those over 50 years old, with a peak incidence in patients who are in their 70s.

Answer 85

raised inflammatory markers ESR > 50 mm/hr (note ESR < 30 in 10% of patients) CRP may also be elevated temporal artery biopsy skip lesions may be present note creatine kinase and EMG normal

Neurology Flashcards

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