Neurology - done Flashcards

(128 cards)

1
Q

What is tPA used for?

A

Thrombolysis after acute ischaemic stroke - NICE says within 4.5hrs, national clinical guidelines for stroke of UK&I considers up to 9hrs

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2
Q

TIA mx

A

Aspirin 300mg daily started immediately (plus ppi if appropriate)
Specialist assessment and investigation within 24hrs
Secondary prevention as soon as diagnosis confirmed

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3
Q

True or false - in Bells Palsy there is forehead sparing.

A

False - in Bells Palsy, there is paralysis of the frontalis muscle which means they cannot raise eyebrows

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4
Q

What is Bells Phemonena

A

When attempting to close the affected eye, the eyeball on the affected side rotates upwards and outwards.

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5
Q

How quickly does Bells Palsy occur

A

Usually within 24hrs, sometimes few days

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6
Q

What happens to the corneal reflex in Bells Palsy

A

The sensory component of the corneal reflex is intact (trigeminal) but the motor component is lost (facial innervation of orbicularis oculi) so the reflex is absent on testing.

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7
Q

What is the prognosis of Bells Palsy

A

70% recover spontaneously, 30% ongoing complications such as ongoing weakness, synkinesis. Usually recovery within weeks but can take up to 6 months if severe.

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8
Q

Examination findings in Bells Palsy

A

LMN facial nerve.
Mouth sagging
Unable to close eye and Bells phenomenon
Loss of taste of anterior 2/3 tongue
Numbness of side of face
Hyperacusis

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9
Q

What is Ramsey hunt syndrome

A

Bells Palsy with ear rash (varicella zoster, treat with antivirals)

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10
Q

Management of bells Palsy

A

Oral steroids (within 72hrs onset) - increases chance of full recovery and reduce sequelae eg. 25mg BD for 10d or 60mg for 5d then reduce by 10mg per day for 5 days to stop.
Antivirals currently not recommended by NICE (unless Ramsey hunt syndrome)
Eye care important

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11
Q

How is parkinsons dementia different to alzheimers in presentation

A

PDD may affect multiple cognitive domains attention memory visuospelacial and exec function. Exec dysfunction tends to occur early and is more commonly found in PDD than Alz.
Psychiatric symptoms less common in PDD compared to in Lewy Body.

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12
Q

First line management parkinsons symptoms affecting QOL

A

Levodopa ( as cocareldopa, Co beneldopa)

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13
Q

What percentage of stroke risk following TIA is in first 48hrs

A

50%

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14
Q

How long does TIA last

A

Technically resolve within 24hrs
But usually less than 1hr and sometimes only minutes

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15
Q

Management of TIA

A

Aspirin 300mg daily to be started immediately
Seen in specialist clinic within 24hrs

This is because secondary prevention is so important to prevent a stroke

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16
Q

Symptoms of stroke

A

Focal cerebral or retinal symptoms lasting seconds minutes or usually less than 1hr
Motor weakness in 2 limbs or 1 limb and face
Sensory deficit in 2 limbs or 1 limb and face.
Homonymous hemianopia, or monocular blindness
Aphasia or dysarthria.

Possibly TIA - unsteady gait, diplopia, vertigo, dizziness

Very rare for TIA to cause LOC, amnesia, confusion, headache etc .

Those with atypical symptoms have bad outcomes because of delay of dx and mx.

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17
Q

How to screen for stroke/TIA

A

Face - weak or numb - ask patients to smile
Arms - weak or numb - ask patients to raise both arms
Speech - ask patient to repeat a sentence.
Time to call 999

In interim, exclude hypoglycaemia if you can! For any sudden onset neurological symptom.

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18
Q

Should you give aspirin if you suspect stroke

A

No . Don’t give aspirin until they have been scanned to ensure not haemorrhagic. Sometimes it is hard to know if TIA or stroke, so in practice, only give the aspirin if the neurological symptoms have completely resolved.

If stroke, immediate admission, ideally scan within 1 hr so more likely to get thrombolysis.

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19
Q

Primary care mx If TIA suspected (neurology completely resolved)

A

Aspirin 300mg immediately then daily
Refer to TIA clinic in 24hrs
Do not use ABCD2
As soon as diagnosis confirmed - secondary prevention - statin.

Secondary care will likely change to long term clopidogrel.

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20
Q

Primary Care mx if suspected stroke (still neuro present)

A

No aspirin until scan
Admit for immediate scanning within 1hr

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21
Q

Secondary care mx (thrombolysis or thrombectomy)

A

Thrombolysis
- haemorrhage excluded
- within 4.5hrs of symptom onset. NCGS go to 9hrs if evidence of salvageable tissue on imaging.

Thrombectomy (can be with thrombolysis if appropriate)
- ASAP and within 6hrs.
- if confirmed occlusion of proximal anterior circulation

6-24hrs post onset
- thrombectomy alone if proximal anterior circulation
- thrombectomy plus thrombolysis if occlusion of posterior circulation (don’t know why?)

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22
Q

Medical mx of strokes immediate

A

Antithrombotic/anticoag choice
If ischaemic stroke
- aspirin 300mg for 2 weeks
- then swap to longer term antithrombotic eg clopidogrel

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23
Q

Management of migraine

A

Sumitriptan can be used acutely
Prophylaxis topiramate, propranolol and amitriotyline.
Topiramate CI in pregnancy.

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24
Q

Prophylaxis of cluster headaches

A

Verapamil

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25
Neuropathic pain mx
Amitriptyline (TCA) duloxetine (SNRI) gabapentin pregabalin
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Presentation of trigeminal neuralgia
Severe unilateral paroxysmal electric shock like facial pain only in the distribution of the trigeminal nerve (not scalp, mandible or ear). Paroxysms of pain (few seconds to 2 minutes). Allodynia. Usually 50-70YO Most patients get good pain relief with carbamazipine. No other options. Often the underlying cause is compression of the trigeminal nerve by a normal blood vessel in the cranium (85%). 5-15% due to secondary causes - MS - Vascular abnormalities - Tumour of cerebellar pontine angle. Secondary causes more likely if younger, associated facial sensory loss, or bilateral pain.
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Symptoms of giant cell arteritis
Headache jaw claudication visual disturbance scalp tenderness
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Diagnosis and mx of GCA
Raised ESR (gp can do) Temporal artery biopsy show multinucleated giant cells Duplex US shows halo sign of temporal artery (these only done by secondary care) If new visual loss - same day assessment by ophthalmologist For all others suspected GCA - Urgent discussion with rheum usually. Ideally same day or within 3 days, specialist review. If strongly suspected GCA, start high dose steroids immediately. 40-60mg oral pred Steroids for 1-2 years or longer!
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What is transient global amnesia
Single episode of dense amnesia lasting less than 8 hrs with complete recovery and without features of epileptic sezirue. Recurrence rate is low. If recurrent episodes, patient should be referred for assessment for epileptic amnesia.
31
What is the most common type of motor neurone disease
ALS (amyotropic lateral sclerosis) is the most common type of MNS. Causes mixed upper and lower motor neurone disease. Primary lateral sclerosis is rate and characterised by ascending spastic tetraparesis. Progressive bulbar Palsy, usually women, typically progresses to anarthria in 6-12m with normal limb strength. Progressive muscular atrophy is least well defined, presents with asymmetrical weakness and wasting often in legs
32
How long after mild head injury can should you rest for ? And when back to contact sport?
48hrs rest Return to work when feel able No contact sport for 3 weeks
33
What condition is most likely to be associate with medication overuse headache
Migraine. Use of triptsns, ergots, combination analgesics for 10d or simple analgesics for 15d is expected to cause a medication overuse headache Need to safely withdraw overused medication. This is done abruptly - withdraw for at least a month. Warn patient other pain condition may get worse.
34
Antithrombotic for secondary prevention of stroke
Clopidogrel first line Second line if allergic or intolerant - aspirin + dipyridamole Aspirin alone if also intolerant of dipyridamole
35
What score to assess stroke risk jn AF
CHA2DS2VASc
36
Essential tremor definition
Bilateral symmetrical intention tremor First line mx propranolol or primidone Refer if not tolerate or if other neuro features
37
Typical features of cluster headaches
Localised pain around the eye associated with lacrimation. Usually once or twice daily for several weeks before resolving. May recur months or years later
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BP control in acute stroke
Haemorrhagic - consider rapid BP lowering if SBP >150 and presents within 6hrs. - consider rapid BP lowering if SBP>220 and presenting >6hrs of onset. If rapid BP lowering, aim to reach SBP <140 but avoid drop of >60 within 1hr of starting treatment. (Not BP lowering if structural cause, GCS6 or less, early neurosurgery, or massive haematoma with poor prognosis) In ischameic stroke- early hypertension mx does not help unless hypertensive emergency! But if thrombolysis, need BP <185t /110 f ischaemic -
40
Statins in acute stroke
Start statin after 48hrs or as soon as swallow is safe.
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When to start anticoagulation after stroke with AF
Treat with aspirin for 2 weeks before switching back to DOAC. This is because of risk of haemorrhagic transformation. (Little evidence for this)
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What is thrombolysis
Clot busting with an IV drug (alteplase or tenectoplase) given within a window of opportunity. Risk of intracerebral haemorrhage.
44
What is thrombectomy
This is endovascular physical removal of the clot by inserting device via femoral artery which can pull out the clot. Only suitable for large vessels. Usually only done after thrombolysis. (Doesn't work well on its own)
45
Secondary prevention after TIA or stroke ischamic
ABCS Antiplatelets - clopdigrel 75mg daily for stroke and most TIAs. NCGS recommends DAPT for 1m if TIA presents within 24hrs. (Aspirin and dipyridamole in clopi allergy). Blood pressure- biggest medically treatable factor! Treat as normal BP guidelines. Aim for clinic BP <140/90 (150/90 if >80YO). AntiCoag - if AF Statins - high intensity, normally atorvastatin 80mg. Treat to target LDL <2 or non-HDL <2.6. Add ezetimibe also to lower CV risk further.
46
Statins after haemorrhagic stroke?
Nice says avoid
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Difference in use between antiplatelets and anticoagulants
Antiplatelets are generally used to reduce arterial thrombotic risk, anticoagulants reduce venous thrombotic risk.
48
What to do if AF and then stroke for secondary prevention
Assuming embolic risk is high enough, anticoagulant for stroke prevention (not antiplatelet). (Secondary care may put patient on both).
49
5 ds of posterior circulation stroke
Dizzy Dysarthric Diplopia Dysphagia Dystaxia
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What medications should be used for neuropathic pain in MS
First line - amitriptyline, duloxetine, gabapentin or pregabalin. Tramadol can be used if acute rescue therapy is needed.
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What psychological treatments are recommended by NICE for chronic pain
CBT and acceptance and commitment therapy
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Opioid induced pruritus stats
occur in up to 10% those on oral up to 50% those with IV up to 100% those with intrathecal or epidural use. Can be managed with ondansetron, diclofenac, antihistamines.
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What is neuroleptic malignant syndrome
Rare but serious idiosyncratic drug reaction. Usually presents with triad of fever, muscle rigidity and autonomic instability, as well as mental status changes. CK is markedly increased, usually 1000-10,000. Also impaired LFTs and U&Es, and ECG abnormalities. Most common cause is exposure to dopamine receptor antagonists eg metoclopramide, prochlorperazine, chlorpromazine, also haloperidol, risperidone, quetiapine. Can also be due to rapid withdrawal from dopamine agonists pramipexole, ropinirole, rotigotine, cabergoline.
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What is the most common type of MND
ALS - 60% cases. Most commonly presents with limb features. PBP is the second most common - difficulties with speech, swallowing.
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DVLA epilepsy/seizures
6 months fit free if isolated single seizure 12 months seizure free if epilepsy T2 licences 5 years and neuro assessment for single seizure without epilepsy medication. 10 years seizure free without epilepsy medication and neuro assessment if epilepsy.
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Which are the safer antiepileptics to be taking if pregnant
Better is lamotrigine and levetiracetam. Need drug monitoring either therapeutic drug monitoring or clinical monitoring. Sodium valproate, carbamazipine, phenobarbital, phenytoin, topiramate have increased risk of major congenital malformations.
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What options are there for chronic neuropathic pain such as painful diabetic neuropathy?
Amitriptyline (TCA) Pregabalin/gabapentin Second line if above doesn't work: Duloxetine
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Management of rapidly progressive symmetrical weakness.
If progressing over less than 4 weeks, may signify potentially life threatening neuromuscular disorder, cervical myelopathy. If progressing within hours to days, consider guillain barre syndrome or transverse myelitis. Needs immediate referal to neurology, for neurological assessment and assessment of bulbar and respiratory function.
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Presentation of guillain barre syndrome
Most commonly presents as progressive ascending muscle weakness and tingling sensations often starting in the legs and spreading to the arms and upper body. Will progress to problems breathing and swallowing if not caught early. If fever think of alternative causes. It is an acute inflammatory neuropathy affecting peripheral nervous system. 66% cases follow URTI or GI infection (triggered by virus or bacteria) Treatment is supportive, some will need respiratory support. IVIg improves outcomes if given within 2 weeks of symptom onset. Mortality 3-10%. 80% regain ability to walk within 6 months. Bimodal distribution of young adults and elderly.
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Diagnosis of motor neurone disease
Based on characteristic clinical symptoms and signs of upper and lower motor neurone degeneration supportive by neurophysiological evidence of motor neurone involvement and exclusion of structural lesions with appropriate MRI. More common in men than women. MND does not cause sensory disturbance.
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Presentation of essential tremor.
Common. Can diagnose if bilateral upper limn action tremor, with or without tremor in other locations (head, larynx voice tremor, or lower limbs). Should be present for 3 or more years to diagnose. No associated neurological symptoms. Often family history as genetic component. Assess for factors which may worsen tremor before diagnosing essential tremor (such as metabolic or hormonal conditions and drug causes).
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Management of essential tremor
Propranolol or primidone depending on patient comorbidities (eg B blockers CI in asthma). Refer if medications do not help.
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How to diagnose MS
Need to have episodes occurring in different places at different times. Therefore history very important. Optic neuritis (unilateral vision loss rapidly worsening over hours to days, often with pain on eye movements, colour vision disturbance and central blind spot scotoma) is a very common presentation. If more than 3 plaques on MRI with optic neuritis, change of MS in future is 75%.
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What to do if patient presents to you with likely functional tremor
Refer to neurology - this diagnosis should be made by specialists.
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What medications can be used for prevention of migraine?
Propranolol Amitriptyline or Topiramate. chose one based on patients preferences, comorbidities.
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What is the characteristic headache in migraine?
On average 1hr to max intensity and lasts 24hrs. Unilateral or can be bilateral, throbbing, worse with activity, can change sides during attack or at next episode. Associated photophobia or phonophobia, allodynia, or N&V. Aggravated by routine ADL, causes activity avoidance. May get premonitory symptoms for hrs-days before (yawning, light sensitivity, nausea, diarrhoea, neck pain, mood changes, tiredness). May get aura usually lasting 60mins, before headache (visual, sensory, speech, motor, or vertigo, or retinal symptoms) - may be positive or negative symptom. May get prodromal period of 12hrs or so after headache before feeling better. Similar to premonitory phase. NB: if strange symptoms in migraine aura, may be something else (TIA, GCA, raised ICP, occipital seizures, retinal detatchment) - if in doubt, refer same day if needed.
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Treatment of acute migraine
Pharma - NICE recommends oral triptan PLUS NSAID/paracetamol for every headache. or monotherapy with oral triptan or aspirin or paracetamol or NSAID if people don't want duel. Add metaclopramide/prochlorperazine if early or persistent vomiting, and can use nasal or SC triptan in these people Non pharma - good hydration, regular meals, sleep, exercise, avoid known triggers. - avoid meds that can make migraine worse - oral contraceptives, HRT, nasap decongestants, SSRIs, PPIs, opioids.
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Prophylaxis for migraine
Start when affecting QOL/frequency of attacks at least weekly, or prolonged severe attacks. Aim to reduce severity and frequency by 50%. Use each treatment at max tolerated dose for 3m before deciding if effective or not. First line options are propranolol, topiramate, amitriptyline. Candesartan unlicensed. Propranolol not in asthma. Topiramate not in pregnancy, B blockers and candesartan also not in pregnancy. Topiramate can cause depression. Non drug options: NICE recommends accupuncture. CBT also recommended. Refer if >3 prophylactic treatments have failed.
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Management of menstrual migraine
Can take triptans off licence for 2 days before until 3 days after bleeding starts. 5 days total. there can be risk of medication overuse headache with triptans especially if used at other times in the month too.
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What to do for migraine in pregnancy
Acute treatment - paracetamol first line. Ibuprofen can be used until 28 weeks but not after 28 weeks. - triptans are the treatment of choice if simple analgesia fails. Can be used throughout pregnancy. be mindful of acute headache in pregnancy - may be pre eclampsia, or cerebral venous thrombosis. Check neuro exam, fundoscopy, and BP and urinalysis.
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Migraine and contraception
If AURA present - COCP if MEC4. Other hormonal contraception MEC2. If no AURA - COCP MEC2 for initiation, MEC3 if develops a new history of migraine whilst taking COCP. This is because migraine is associated with increased risk of ischaemic stroke (2-4 times increase) and this is highest if aura. transdermal HRT fine with migraine.
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Red flags for headaches
HEAD CRISIS C Head trauma last 3 months Exacerbated by cough/valsalva/ sneezing/exercise/change in posture Acute narrow angle glaucoma /GCA Deficit (neurological), cognitive impairment or change in personality. Change in character of headache Roasting hot (fever with worsening headache) Impaired consciousness Sudden onset (max intensity within 5 minutes) - immediate ref to exclude SAH. Immunocompromised Sick (vomiting) without an obvious cause Cancer - previous cancer known to metastasise to the brain, or <20YO with cancer history.
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First thing to do to investigate headaches
Exclude red flags Then headache diary for 8 weeks
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Typical presentation of cluster headache
Unilateral only! around the eye and along side of face severe/very severe lasts 15mins- 3hrs. Can get many episodes within a day. May get automonic features on same side eg sweating/red watery eye/constricted pupil/swollen or drooping eyelid, nasal congestion. May be restless/agitated. Refer to confirm diagnosis May occur once every 2 days or up to 8 times daily. If episodic, get pain free periods more than 1 month. If chronic, don't get the pain free periods.
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Typical presentation of tension headache
Bilateral, pressing/tightening, not pulsatile. Mild to mod severity, can last anywhere from 30mins to continuous. No associated symptoms. Not aggravated by ADLs. Can be episodic or chronic. Treat with paracet/nsaid or asprin (not if under 16YO due to risk of reye syndrome). Not opioids. Warn of medication overuse headaches. Can use acupuncture for prophylaxis.
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Typical presentation of medication overuse headache
Location, severity and duration all variable. Consider if frequent use of acute treatment for headache for more than 3 months of: - paracet, NSAID or aspirin >15d/m - triptan, opioid, ergot or combination analgesia >10d/month. Not aggrevated by ADL.
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Management of cluster headaches
Acute treatment 100% oxygen NRB mask OR subcut or nasal triptans Paracetamol/NSAIDs/oral triptans/opioids/ergots all do not work! Warn about risk of medication overuse headache Prophylaxis Verapamil may help. Refer for diagnostic clarification. May need imaging. Non invasive vagus nerve stimulators may be initiated in secondary care.
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What is cervicogenic headache?
Headache due to neck problem. Needs to have neck problem and at least 2 of onset of headache related to onset of neck problem, headache improves/resolves with improvement of neck problem, ROM is reduced and headache worse with certain neck movements. Headache will resolve with nerve block of cervical structure.
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What is medication overuse headache
Headache 15d/month while taking regular acute headache treatment for more than 3 months (more than 15 days per month if simple analgesia, more than 10 days per month if triptans, combined analgesia, opioids or ergots). triptans and opioids most common cause. It only occurs if acute analgesia meds is used for underlying headache disorder, not if using for another painful condition. RF is frequent headache, frequent acute medication, pain from another cause, mental health condition. Self perpetuating as more headache then takes more analgesia.
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Treatment of medication overuse headache
Prevention better than cure, advise not to use any medication for more than 2 days per week. Discuss overuse headache with anyone taking regular acute medication for headache disorder. Stopping overused medication can reduce headache freq and severity but headaches may worsen before they get better (1-2weeks). NICE advise to stop all overused drugs for at least 1 month, abruptly. Warn of short term deterioration likely. Offer support/FU through this period. Then review at 4-8 weeks and consider prophylactic management of underlying headache disorder.
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When should headache make you think of raised ICP
Raised ICP is medical emergency (and symptom of something else going on). Consider if any of: 1. new onset headache/near constant headache, severe headache or change in headache pattern. 2. Visual disturbance 3. Papilloedema 4. Pulsatile tinnitus Refer that day if headache and papilloedema/visual disturbance. Untreated raised ICP can cause permanent sight loss/neurological deficits and death. May also have neck or back pain, lethargy, weakness, behaviour changes, vomiting, reduced consciousness, seizures, sepsis, headinjury, history of cancer.
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what should be included in primary care assessment of headache ?ICP
Good history blood pressure Full neuro exam including cranial nerves and visual fields. Fundoscopy.
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When to do same day referral for headache?
Headache with papilloedema - needs neuroimaging Headache and visual disturbance - need formal visual field testing.
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What is MS?
Acquired chronic inflammatory condition of CNS. Commonest age of presentation 20-30YO. Most common serious physical disability of working aged adults.
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What are the three types of MS?
Relapsing remitting - most common, 85% have this initially. Secondary progressive - over time, half people with RR MS develop secondary progressive. Gradually worsening of disability Primary progressive - rare, 15%, gradually worsen with no relapses or remissions.
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Presentation of MS
Most commonly visual/sensory disturbance, limb weakness, gait problems, bladder or bowel dysfunction. Visual disturbance may be loss or reduced vision in one eye, with painful eye movements, loss of red discrimination (optic neuritis), or double vision. Sensory symptoms is ascending sensory disturbance or weakness. More likely to be MS with neurological symp/signs if aged under 50, no fever/infection, symptoms evolving over more than 24hrs, persist over several days/weeks and then improve, and may have history of previous neurological symptoms. Need to rule out alternative causes depending on the presentation.
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What 3 specific instances of when to consider MS
Rapidly progressive unsteady gait - urgent neurology referral. Progressive memory problems in young adult with multiple cognitive functions - routine referral. Persistent distally predominant altered sensation in limbs with brisk deep tendon reflexes - routine referral. Things not suggestive of MS - fatigue, depression, dizziness, vague sensory symptoms without focal neurological signs or symptoms, headache.
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What is MS prodrome
In 10 years before diagnosis, those with MS often have non specific consultations to the GP - with GI and urinary symptoms, depression, anxiety, insomnia, pain. This is prodrome when looking with hindsight but cannot tell at time.
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what is optic neuritis
Inflammation of the optic nerve. Partial or total unilateral visual loss developing over a few days, eye pain (in particular on eye movement) and/or loss of colour vision (particularly reds). May be bilateral. Need to ensure not neuromyelitis optica (rare alternative demyelinating disorder, high mortality rate if not treated with immunosuppression). If thinking about optic neuritis, refer to neurology.
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How to diagnose MS
Secondary care done. Based on history, examination, MRI and laboratory findings. Not diagnosed on MRI again.
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DVLA for multiple sclerosis and MND.
Must notify DVLA and can drive as long as safe vehicle control maintained. Licence for 1 2 3 or 5 yrs may be issued provided medical enquiries by DVLA confirm driving performance is not impaired. May need specific controls. Same for group 2.
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Long term follow up for MS
All under secondary care. Yearly review. Including symptoms and functional impact, MS disease course, general health including smoking/weight/exercise etc, medication review, bone health. Risk of contractures and pressure ulcers. Care and carer needs.
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Treatment for MS
DMARD treatments - reduce relapses. They can be associated with blood abnormalities, increased risk of infection, cardiac arrhythmias, macula oedema, secondary autoimmunity, and in some cases increased risk of cancer. If women of childbearing age - need contraception. Avoid live vaccines.
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Common long term symptoms in MS
Fatigue, mobility problems, spasticity, oscillopsia, emotional lability, pain, cognitive and memory problems, ataxia, dystonia and tremor.
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Potential management of spasticity in MS
May use spasticity to maintain posture and using medication may impair this. First line - baclofen Second line - gabapentin Third line - both together.
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Urinary symptoms in MS
May get overactive bladder or stress incontinence For overactive bladder - antimuscarinics (however, may worsen CI in MS) - bladder wall botox injection if antimusarinics not tolerated or not effective. Stress incontinence - PFME
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What does an MS relapse look like>
If person with stable disease then develops new symptoms or worsening of existing symptoms and these last more than 24hrs. Need to exclude infection eg chest infection, UTI. Commonest symptoms of relapse include optic neuritis (loss of visual acuity), sensory alterations, weakness, imbalance, and fatigue and cognitive dysfunction. Usually relapse occurs over hours to days then reaches plateau which may last days to weeks. Recovery may be complete or incomplete, and may take months. refer to secondary care if suspected relapse, they will usually give oral or IV methylprednisolone.
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How can relapses be prevented in MS?
DMARDs exercise is beneficial not smoking. immunisations
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Drugs that can cause tremor
Antidepressants, lithium, valproate, theophylline, thyroid hormones, immunosuppressants, caffiene, nicotine, glucocorticoids, sympatheticomimetics (adrenaline, salbutamol, cocaine, MDMA, amphetamines).
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What type of tremor in essential tremor
Postural or kinetic tremor. Usually upper limbs, bilateral, may also have tremor in head, larynx or lower limbs. Medium fast
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Management of essential tremor.
devices such as weighted pens or computer mice can help tremor. other devices can help with buttons, drinking and eating. pharma mx with propranolol or primidone. Can use together.
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Typical signs and symptoms of carpal tunnel
Compression of median nerve at the wrist. Most common compression neuropathy in primary care. Distribution is palm and lateral 3.5 digits. Pain and paresthesia. Median nerve also supplies motor fibres to thenar eminence so CTS can cause wasting of this. Symptoms often intermittent. Pressure on the median nerve can cause demyelination too. Pain and tingling wakes at night, more pronounced first thing in the morning. Often people have movements to make the tingling go away.
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Risk factors for CTS
twice as common in women. increases over age 30 Obesity, diabetes, RA, previous wrist fracture, use of walking stick. Weaker risk factors include smoking, hypothyroidism, keyboard use, and racquet sports.
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How to diagnose carpal tunnel syndrome?
Gold standard would be nerve conduction studies. However in primary care can do Kamath and Stothard scored questionnaire - clinician administered. This asks about about symptoms, pattern, affect of pregnancy and of wearing splint. Need score of 5 for CTS. Special tests Phanels, Tinnels, Durkans, have poor sensitivity and specificity and should not be used. Nerve conduction studies generally only done if considering surgery. Blood tests only required if possible secondary cause eg thyroid disease or RA.
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What would be the differential of CTS
Cervical radiculopathy (especially if bilateral). Cubital tunnel syndrome - ulcer nerve compression usually at elbow (this causes little finger symptoms). Less commonly peripheral neuropathy, cervical cord disease (MS), raynauds. Could also be MND, acute stroke. NB: de quervains tenosynovitis causes pain in the hand or wrist but not usually sensory disturbance.
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Primary care treatment of CTS
Conservative management options 1. Wrist splint at night - limited effectiveness 2. Single corticosteroid injection (evidence that this is more effective than splints). Should get improvement within 6 weeks. refer to secondary care if persisting symptoms or disability not responding to 6 weeks of conservative mx. Don't delay secondary care referral as surgical outcomes poorer if longer period of symptoms.
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What is surgical mx for Carpal tunnel syndrome
Open or endoscopic decompression. Most respond well, only minority require rehab post op. Recurrence rate up to 10%.
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What is cubital tunnel syndrome
This is entrapment of the ulnar nerve in the cubital tunnel (funny bone). Affects ring finger and little finger. This is second most common mononeuropathy. Left untreated will progress to motor symptoms due to atrophy of small intrinsic muscles of the hands. Must less commonly the ulnar nerve can be trapped at the wrist which is called Guyon canal syndrome .
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How to diagnose cubital tunnel syndrome
Clinical diagnosis (but no validated scoring system like we have for carpal tunnel). may be confirmed by US or nerve conduction studies.
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Management of cubital tunnel syndrome
Education Avoiding aggrevating activities (prolonged resting on elbows). Elbow splinting, braces and nerve gliding exercises have been suggested. All lack supporting evidence. Surgical decompression in refractory cases.
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Drugs to avoid in parkinsons
Metoclopramide Prochlorperazine Perphenazine Flupentixol Chlorpromazine Fluphenazine Haloperidol Pimozide Sulpiride Trifluoperazine
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Which screening test is recommended by NICE for cognitive impairment
6CIT
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Considerations regarding epilepsy in older people
More likely to have underlying organic cause eg tumour stroke Alzheimer's More likely to start medication after single seizure due to increased risk of future seizure. Levetiracetam or lamotrigine usually first line.
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Commonest cause of foot drop
Weakness of muscles of dorsiflexion of the ankle, causing problems with walking. Commonest cause peroneal neuropathy, mostly due to external pressure on the nerve eg cast wearing, leg crossing, prolonged kneeling or squatting. Can also be due to nerve root disease (ask about back pain) or nerve disease, or myopathy, or stroke, musclular dystropy (but latter two are rare and would present with other things too). Differentiate based on pattern on neuro exam. EMG or nerve conduction studies to confirm working diagnosis of peroneal neuropathy. Behaviour modification as management. Consider orthosis to help support foot, maybe PT. Refer if not improving in primary care. If bilateral foot drop - refer - ?CAS.
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Idiopathic normal pressure hydrocephalus
Few potentially reversible causes of dementia so important to consider diagnosis. Will have ventriculomegaly without raised CSF pressure. Can also get normal pressure hydrocephalus with other conditions such as SAH or meningitis. Presents in those over 60 with gait and balance disturbance, cognitive impairment and urinary incontinence. No not all may get all features. Dementia or Parkinson's key differentials. If suspected, refer to neuro for neuroimaging. Treat with VP shunt.
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Risk factors of MND
Presentation 50-60YO, commoner in males. 10% genetic. Link with physical activity especially if concussive or cervical trauma. Early diagnosis prolongs survival
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Presentation of MND
Progressive muscle weakness (and wasting) without significant sensory component. 70% present with limb symptoms. asymmetrical, twitching, fasciculations, wasting, cramps, often distally. 25% present with bulbar symptoms (dysarthria quiet hoarse slurred speech, espeically if tired. also dysphagia liquids more than solids). Wasted tongue, excessive saliva, tongue fasciculation. Urgent referral if swallow affected. Also get respiratory features (especially later) and cognition affected. When referring - specifically mention you are considering MND. 50% of those with ALS will develop cognitive impairment, 80% anxiety, 20% psychosis. Not affected in MND: bladder/bowel, sensory, vision. Also any symptoms that improve goes against MND - it is always progressive.
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Types of MND
ALS most common 85%. Mixed UMN and LMN. Survival mean 4yr from symptom onset. Primary lateral sclerosis - rare 3%, UMN dysfunction and substantial spasticity but best survival rates. Primary muscular atrophy - LMN with muscle atrophy and flaccid paralysis. Survival between ALS and PLS. Mx to alleviate symptoms, maintain function, ACP. Single drug Riluzole is licenced for ALS - modest benefit at improving survival but doesnt improve symptoms.
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Some drug options for symptoms of MND
Muscle cramps - quinine, baclofen Spasticity - baclofen, dantrolene, tizanidine Drooling - conservative then antimuscarinic or glycopyrronium. Gastrostomy for nutrition. DO SR1 form for fast track benefit support.
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Which patients with trigeminal neuralgia should be referred?
Less than 40, bilateral symptoms, opthalmic division only, sensory loss, hearing loss, skin or oral lesions, optic neuritis or FHx of MS, poor response to treatment (consider surgery). If facial pain and persistent facial numbness - refer 2WW for infiltrative/intracranial mass. If facial pain and headache - same day assessment for GCA.
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Side effects and considerations with carbamazepine for trigeminal neuralgia
Side effects common - dizziness, diplopia, ataxia, elevated LFTs, hyponatraemia. Enzyme inducer so multiple drug interactions. Bloods at intiation but routine blood monitoring not required. NB some asian populations have allele HLAB1502 that increases risk of SJS with carbamazipine, so do genetic testing before prescribing in these people. If patient does not respond to carbamazipine, refer. They may get radiosurgery.
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Can functional neurological disorder be diagnosed in primary care
No, unlike IBS and fibromyalgia, everyone with suspected functional neurological disorder should be referred to secondary care for assessment and diagnosis. Symptoms of FND may include motor or sensory symptoms, sleep disturbance, memory problems, dissociative symptoms, seizures. Often multiple symptoms across multiple body areas. Previous adverse experiences are risk factors. Might have variability. Often co-exist with another neurological condition eg epilepsy, MS.
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MX of functional neurological disorder
Communicate diagnosis well Physiotherapy and other rehab Psychological therapy Drug treatments - SSRI if concurrent MH problem but not only for FND. Comorbid conditions - treat actively where possible. If new symptoms or signs - refer back for neurological assessment.
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Red flags for vertigo
Bidirectional, torsional or vertical nystagmus are bad. Negative head impulse test (Positive test if there is saccade, this means peripheral rather than central, therefore negative HIT indicates more likely central cause). Any skew deviation (corrective movement in uncovered eye) needs urgent referal for possible central cause. Other neurological deficits - one sided deafness, dysarthria, severe gait ataxia. Limp abnormalities such as numbness, weakness, poor coordination.
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Differential diagnosis vestibular migraine
Neuro - posterior stroke, demyelination Local- cervical dizzness ENT - BPPV labyrinthitis, menieres Other - anaemia, diabetes, hypovolaemia, psychosomatic disorder.