Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

3a > Neuro > Flashcards

Neuro Flashcards

1
Q

What is a TIA?

A

Brief episode of neurological dysfunction due tot temporary focal cerebral ischaemia without infarction.
Symptoms have generally resolved after 24hrs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Risk factors for TIA?

A
  • Age
  • HTN
  • Smoking
  • Diabetes
  • AF
  • Prev TIA
  • Hyperlipidaemia
  • Vasculitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where do most TIAs affect?

A

Anterior Circulation 90%: Frontal and medial cerebrum.

Posterior circulation 10%:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is amaurosis fugax?

A

Sudden transient loss of vision in one eye. Due to temporary reduction in retinal, opthalmic or cilliary blood flow. Causes temporary retinal hypoxia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Clinical features of TIA?

A 
Anterior:
- Weakness of limb
- Hemisensory disturbance
-Dysphasia
- Amaruosis fugaz
Posterior:
- Diplopia
- Vertigo
- Choking and dysarthria
- Ataxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Investigations of TIA?

A 
Bloods : To check for cause
Carotid artery USS
MRI/CT angiography
ECG
ECHO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Scoring system in TIA?

A 
ABCD2,
Age>60 
BP>140/90
Clin featutres: 
- Unilateral weakness = 2
- Speech disturbance only = 1
Duration:
- >1hr = 2
- 10-59mins = 1
Diabetes

> 6 stroke likely. Tx Refer urgent.
4 see specialist in 24hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Medications used in TIA?

A 
Antiplatelets:
 - Aspirin and dypyramidole then lower dose
- Clopidogrel long term
Warfarin
Statins. ACe-i, etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a stroke?

A

Syndrome of rapid onset of neurological deficit caused by focal cerebral, spinal or retinal infarction.Characterised by rapidly developing signs of focal or global disturbance lasting more than 24 hrs or leading to death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What can cause haemorrhagic stroke?

A
  • Trauma
  • Aneurysm rupture
  • Anticoagulation
  • Thrombolysis
  • Carotid artery dissection
  • SAH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a watershed stroke?

A
  • Sudden drop in BP, low cerebral blood flow and global ischaemia. Watershed infarcts in vulnerable areas between boundaries of arterial territories. Seen in sepsis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Presentation of Anterior Cerebral Artery stroke?

A
  • Leg weakness
  • Gait apraxia
  • Truncal ataxia
  • Incontinence
  • Akinetic mutism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

presentation of Middle Cerebral Artery stroke?

A
  • Contralateral arm and leg weakness
  • Contralateral sensory loss
  • Hemianopia
  • Aphasia
  • Dysphasia
  • Facial droop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Presentation of posterior cerebral artery stroke?

A
  • Contralateral homonymous hemianopia (loss of half vision of same side in both eyes)
  • Cortical blindness
  • Visual agnosia
  • Prosopagnosia
  • Colour naming problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Presentation of posterior circulation - vertebrobasillar artery?

A
  • “Locked in”
  • Motor deficitis (hemiparesis, tetraparesis, facial paralysis)
  • Dysarthria
  • Vertigo
  • N+V
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is lacunar stroke?

A

Small subcortical strokes, one of:

  • Unilateral weakness of face and arm, arm and leg or all
  • Pure sensory loss
  • Ataxic hemiparesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Diagnosis of stroke?

A
  • Urgent CT head/MRI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Treatment of stroke?

A
  • Maximise reversible ischaemic tissue: Hydrate, give o2
  • Thrombolysis: IF ISCHAEMIC. IV Alteplase. Up to 4.5hrs post-onset.
    If haemorrhagic: Reverse anticoagulants with Vit K + Beriplex.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are C/I of IV Alteplase?

A
  • Recent surgery 3/12
  • Recent arterial puncture
  • Hx of active malignancy
  • Evidence of brain aneurysm
  • Pt on anticoagulants
  • Severe liver disease
  • Acute pancreatitis
  • Clotting disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is EDH?

A

Collection of blood between the dura mater and the bone usually caused by head injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the causes of EDH?

A
  • Traumatic head injury = Fracture of temporal/parietal bone = Laceration of middle meningeal artery.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Clinical presentation of EDH?

A
  • Head injury
  • Brief post-traumatic LoC or drowsiness
  • Lucid interval (can last several hours/days)
  • Severe headache, N+V, confusion, seizures
  • Ipsilateral pupil dilates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Diagnosis of EDH?

A
  • CT head: Hyperdense biconvex LEMON shaped haematoma.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Treatment of EDH?

A
  • IV Mannitol if icnreased ICP

- Neuro surgery ( Clot evacuation +/- ligation of vessel)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is seen on CT of EDH?

A
  • Lemon shaped haematoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is subdural haematoma?

A

Caused by the accumulation of blood in the subdural space. Between the arachnoid and the dura mater. Following rupture of a bridging vein between cortex and venous sinus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

RF of SDH?

A
  • Traumatic head injury
  • Cerebral atrophy - increasing age / dementia
  • Alcoholism
  • Babies with trauma

Trauma can happen up to 9 months ago.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Presentation of SDH?

A
  • Interval between injury and sx
  • Fluctuating consciousness
  • Headache
  • Sleepiness
  • Raised ICP signs: Headache, vomiting, seizure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Diagnosis of SDH?

A
  • CT : Crescent shaped haematoma. Sickle shaped.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Treatment of SDH?

A
  • Neurosurgery: Irrigation/evacuation via burr twist drill

- IV mannitol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is SAH?

A

Spontaneous bleeding into the subarachnoid space - between the arachnoid layer of the meninges and the pia mater.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Causes of SAH?

A

> Rupture of saccular aneurysms (80%) :
- Rupture of junction of Posterior Communicating artery with the ICA or ACA with ACA

> Atriovenous malformation

> Bleeding disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Risk factors for SAH?

A
  • Hypertension
  • Aneurysm known
  • Smoking
  • Alcohol
  • FH
  • Coagulation disorder
  • Coarc of aorta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Clinical presentation of SAH?

A
  • Sudden onset severe occipital headace (thunderclap headache)
  • Vomiting
  • Collapse
  • Seizures
  • Decreased consciousness
    -Kernigs and burdzinskis signs
  • Papilloedema
    Can have Sentinel headaches before due to warning leak.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Diagnois of SAH?

A
  • Head CT: Star shaped lesion
  • CT angiography to see aneurysm
  • LP if CT normal but SAH suspected.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is seen in LP in SAH?

A

Xanthrochromia due to breakdown of Hb in CSF. Confirms SAH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Treatment of SAH?

A
  • Nimodipine (CCB) reduces vasospasm
  • Endovascular coiling: First line tx for aneurysm.
  • Intercranial stents
  • Balloon remodelling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Complications of SAH?

A
  • Rebleeding
  • Cerebreal ischaemia due to vasospasm
  • Hydrocephalus
  • Hyponatraemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is a migraine?

A

Recurrent throbbing headache often preceded by an aura and associated with nausea, vomiting and visual change.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are triggers of migraine?

A 
Chocolate
Hangovers
Orgasms
Cheese
Oral Contraceptives
Lie ins
Alcohol
Tumult (loud noise)
Exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Risk factors for Migraine?

A
  • genetic component
  • Female
  • Age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Clinical presentation of migraine without aura?

A 
May be prodrome that precedes headache by hours/days: Consists of yawning, cravings, mood/sleep changes.
- 4-72hrs
Two of:
   - Unilateral 
   - Pulsing
   - Moderate/severe pain in head
   - Aggravated by physical activity
At least one of:
   - N+V
   - Photophobia
   - Phonophobia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Clinical presentation of migraine with aura?

A

May be prodrome that precedes headache by hours/days: Consists of yawning, cravings, mood/sleep changes.
At least two attacks.
Aura precedes the attack by minutes and may persist during it:
- Visual: Chaotic lines, scotoma, hemianopia
- Somatosensory: Parasthesia from fingers to face
Unilateral pulsatile headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Diagnosis of migraine?

A 
Exclusion of:
- SAH (do LP)
- SoL (papilloedema, other raised ICP signs)
Red flags:
- Worst headache
- change in pattern of migraine
- Abnormal neuro exam
- Onset over 50
- Epilepsy
- Posterior located headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Treatment of migraine:

A 
- Reduce triggers
Acute: 
   - Triptans eg Sumatriptan 
   - NSAIDs eg Naproxen, asprin
   - Can use anti-emetic: Prochlorperazine
Prevention:
   - Beta blocker eg Propanolol
   - TCA eg Amitryptyline
   - Anti-convulsant eg Topiramate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Side effects of triptans?

A

Arrhytmias
Angina
MI
C/I in: IHD,, coronary spasm, uncontrolled HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is a tension headache?

A

Most common chronic daily and recurrent headache

- episodic or chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

RF for tension headache?

A
  • stress
  • sleep deprivation
  • bad posture
  • hunger
  • eye strain
  • anxiety
  • noise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Clinical presentation for tension headache?

A 
Usually has 1 of the following;
- bilateral
- pressing/tight
- mild/moderate intensity
- +/- scalp muscle tenderness
Without
- vomiting
- sensitivity to head movement
- aura

tight band-like sensation
30mins-7days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Tx for tension headache?

A

lifestyle advice (e.g. regular exercise and avoid triggers)

  • aspirin
  • paracetamol
  • NSAIDS
  • consider TCA (e.g. amitriptyline)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is a risk of using analgesia everyday for tension headaches?

A

Medication overuse headaches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

RF for cluster headache?

A
  • smoker
  • male
  • adults affected mostly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Clinical presentation of cluster headache?

A
  • abrupt onset, excruciating pain around one eye, temple or forehead
  • ipsilateral, cranial, autonomic features
    > blood shot/watery eye with lid swelling and lacramation
    > facial flushing
    > rhinorrhea
    > miosis +/- ptosis
  • pain (strictly unilateral)
  • rises to crescendo over minutes
  • lasts 15-160mins
  • often nocturnal/early mornings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Tx of cluster headache?

A

ACUTE

  • analgesics have NO role
  • 100% 15L O2 for 15mins
  • triptan (e.g. sumatriptan)

PREVENTION

  • CCB (e.g. verapamil - 1st line prophylaxis)
  • avoid alcohol
  • corticosteroids may help
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What nerve is affected in trigeminal neuralgia?

A

Trigeminal nerve (CN5)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is trigeminal neuralgia?

A

Chronic debilitating condition resulting in intense and extreme episodes of facial pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Causes of trigeminal neuralgia?

A
  • Usually due to compression of trigeminal nerve by loop of vein or artery
  • can be due to local pathology (e.g. aneurysms, meningeal inflammation or tumours)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Clinical presentation of trigeminal neuralgia?

A
  • almost always unilateral
  • at least 3 attacks of unilateral face pain
  • facial pain occurs in one or more distributions in trigeminal nerve with no radiation beyond trigeminal distribution
  • pain has at least 3 of the following features:
    > reoccurring in paroxysmal attacks for a fraction of a second - 2mins
    >severe intensity
    >electric-shock-like shooting/stabbing
    > precipitated by innocuous stimuli *e.g. washing/shaving)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Diagnosis of trigeminal neuralgia?

A

Need to be at least 3 attacks with unilateral face pain

MRI to exclude secondary causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Tx of trigeminal neuralgia?

A
  • Typical analgesics and opioids do NOT work
  • Anticonvulsants (e.g. carbamazepine) suppress attacks
  • others: gabapentin, lamotrigine
  • surgery: gamma-knife surgery + microvascular decompression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is GCA/temporal arteritis?

A

Systemic autoimmune-mediated vasculitis affecting medium - large arteries of aorta and its extra cranial branches
- assoc with PMR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

RF for GCA?

A
  • caucasian
  • elderly woman
  • PMR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What type of inflammation is in GCA?

A

Granulomatous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Clinical presentation fo GCA?

A
  • Severe headaches (temporal, pulsing)
  • scalp tenderness
  • jaw claudication
  • tenderness + Swelling of 1 or more temporal arteries
  • sudden, painless vision loss
  • malaise, lethargy, fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How is GCA diagnosed?

A

criteria 3 or more of:

  • over 50
  • new headache
  • temporal artery tenderness or decreased pulsation
  • ESR raised
  • abnormal artery biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the definitive test for GCA?

A

Temporal artery biopsy

  • shows granulomatous inflammation. breaking of internal elastic lamina and infiltrate of white cells
  • do biopsy before or within 7 days of high dose corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Tx of GCA?

A
  • High dose corticosteroids (E.g. oral prednisolone)

- lansoprazole + alendronate to prevent steroid SE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is guillan-barre syndrome?

A

An acute inflammatory demyelinating ascending polyneuropathy affecting the peripheral nervous system (Schwann cells targeted) following an upper respiratory tract infection or GI infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Causes of GBS?

A
  • campylobacter jejuni
  • CMV
  • Mycoplasma
  • zoster
  • HIV
  • EBV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

RF for GBS?

A
  • Hx of respiratory or GI infection (1-3 weeks prior to onset)
  • Vaccinations
  • Post-pregnancy incidents increases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Clinical presentation for GBS?

A
  • 1-3 weeks post infection
  • symmetrical ascending muscle weakness
  • proximal muscles more affected (E.g. trunk, resp, CN)
  • pain is common
  • sensory signs include parasthesia, reflexes lost
  • autonomic features: sweating, raised pulse, BP rise, arrythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Diagnosis of GBS?

A
  • nerve conduction studies (slowing of conduction, prolonged distal motor latency)
  • LP (CSF raised protein and raised WCC)
  • Spiromtery (monitor FVC)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Tx of GBS?

A

If FVC <80% then ventilate + take to ICU + IVIG for 5 days (CI in pt with IgA deficiency)

Plasma exchange
LMWH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is epilepsy?

A

the recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting in seizures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Causes of epilepsy?

A
  • 2/3rds idiopathic
  • cortical scarring
  • SOL
  • Stroke
  • tuberous sclerosis
  • alzheimers
  • alcohol withdrawal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

RF for epilepsy?

A
  • fam hx
  • premature baby
  • abnormal blood vessels in brain
  • alzheimers
  • drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

how can seizures be classified?

A

Primary generalised (40%)

  • Simultaneous onset of electrical discharge throughout cortex
  • Bilateral symmetrical
  • Always assoc with loss of consciousness/awareness

Partial/focal seizures (60%)

  • focal onset with features referrable to part of one hemisphere
  • may later become generalised
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Clinical presentation of generalised clonic-tonic seizure?

A
  • LOC
  • tonic: rigid, stiff limbs, person falls
  • clonic: generalised, bilateral, muscle jerking
  • eyes open, tongue bitten, incontience, followed by period of drowsiness + confusoin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Clinical presentation of typical absence seizure?

A
  • disorder of childhood
  • stops activity, stares and pauses for a few seconds only
  • assoc with 3Hz spikes on EEG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Features of a myoclonic seizure?

A
  • Sudden isolated jerk of limb, face or trunk

- patient may be thrown to ground or have violent disobedient limb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Features of a clonic seizure?

A
  • sudden, sustained increased tone with a characteristic cry/grunt
  • stiffing not followed by jerking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Features of akinetic/atonic seizure?

A
  • sudden loss of muscle tone and sensation of movement causing a fall
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Features of a simple partial seziure?

A
  • not affecting consciousness or memory
  • awareness unimpaired with focal motor, sensory, autonomic or psychic symptoms
  • no post-ictal symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Features of a complex partial seizure?

A
  • affecting awareness/memory before, during or after seizure
  • most commonly arise from temporal lobe
  • post-ictal confusion common
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

features of a partial seizure with secondary generalisation?

A
  • focal electrical disturbance spreads causing secondary generalised seizure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

features of seizure in temporal lobe?

A
  • aura
  • anxiety
  • out of body experience
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

features of seizure in frontal lobe?

A
  • motor features (posturing or pedalling leg)
  • Jacksonian marches
  • post-ictal Todd’s palsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

features of parietal lobe seizure?

A
  • sensory disturbances
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

features of occipital lobe seizure?

A
  • visual phenomena
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

what is a Jacksonian march?

A

seizure marches up or down motor homunculus (starting at face or thumb)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

what features of a seizure point towards epilepsy rather than syncope?

A
  • tongue biting
  • head turning
  • muscle pain
  • LOC
  • cyanosis
  • post-ictal symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

what features of a seizure point towards syncope rather than epilepsy?

A
  • prolonged upright standing
  • sweating prior
  • nausea
  • pre-syncopal Sx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

features of non-epileptic seizures?

A
  • situational
  • longer (up to 20 mins)
  • closed mouth/eyes
  • pelvic thrusting
  • non incontinence or tongue-biting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

diagnosis of epilepsy?

A

To make clinical diagnosis from Hx there needs to be 2 or more unprovoked seizures occurring >24hrs apart to diagnose.

  • EEG
  • MRI
  • CT head (SoL or structural abonormalities)
  • bloods (metabolic causes)
  • genetic testing (Juvenile myoclonic epilepsy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

emergency Tx of epilepsy?

A
  • check glucose
  • if prolonged >3mins or repeated = rectal diazepam
  • IV phenytoin loading
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

tx of primary generalised seizure?

A

generalised tonic-clonic

  • oral Sodium valproate
  • oral lamotrigene
  • oral carbamazepine

absence

  • valproate
  • lamotrigene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What is a SE of sodium valproate?

A
  • weight gain

- hair loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Tx of partial/focal seziure?

A
  • carbamazepine (first line)
  • sodium valproate
  • lamotrigine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

what organsiation should be contacted if someone is diagnosed with epilepsy?

A

DVLA

- have to be seizure-free for 1 year before you can drive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What are the RF for a primary brain tumour?

A
  • ionising radiation
  • vinyl chloride
  • immunosuppression
  • fam Hx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What are the majority of brain tumours?

A

Gliomas

  • astrocytomas (85-90%)
  • oligodendroglioma (5%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What will all gliomas progress to?

A

Glioblastoma multiform

- except pilocyticastrocytoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is a tumour?

A

Malignant or bengin

Act as SoL within the brain and thus result in raised ICP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What are the 4 cardinal presenting symptoms of brain tumours?

A

1) symptoms of raised ICP
2) progressive neurological deficit
3) epilepsy/seizure
4) lethargy/tiredness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What are symptoms of raised ICP?

A
  • Progressive headaches, worse on waking from sleep (aggregated by coughing, straining and relieved by vomiting)
  • Drowsiness
  • Papillodema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Diagnosis of brain tumours?

A

CT/MRI
Biopsy (determine grade + confirm)

DO NOT DO LP –> RISK OF CONING

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Tx for brain tumour?

A

Surgery to remove mass if poss
Chemo for glioma
Oral dexamethasone (Reduced inflammation/odemea)
Anticonvulsants for epilepsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What common cancers metastasise to CNS?

A 
Lung
Breast
Melanoma
Renal cell
GI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What are the anatomical effects of a mass lesion?

A
  • local deformity + shifted structures
  • decreased vol of CSF
  • pressure gradients cause internal herniation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Where does the spinal cord extend from?

A

C1-L1/L2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What is the cauda equina?

A

Lumbar and sacral nerve roots below L1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is paraplegia?

A

Paralysis of both legs, always caused by spinal cord lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What is hemiplegia?

A

Paralysis of one side of body caused by lesion of brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What does the corticospinal tract do?

A
  • motor
  • descending upper motor neurone
  • decussates at medulla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What does the dorsal column do?

A
  • ascending sensory tract
  • proprioception, vibration + 2-point discrimination
  • decussates at medulla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What does the spinothalamic tract do?

A
  • ascending sensory tract
  • pain + temp
  • decussates in spinal cord
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

what are UMN signs?

A
  • signs are contralateral to lesion
  • increased muscle tone (spasticity) (hypertonia)
  • flexors WEAKER than extensors in legs
  • flexors STRONGER than extensors in arms
  • hyperreflexia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

what are LMN signs?

A
  • signs are ipsilateral to lesion
  • decreased muscle tone (hypotonia)
  • wasting +/- fasciculations
  • weakness
  • reduced or absent reflexes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

what is spondyloisthesis?

A

Slippage of one vertebra over the one below
- nerve root comes out above the disc, therefore the root affected will be the one BELOW the disc herniation (e..g L4/L5 herniation leads to L5 nerve root compression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What is spondylosis?

A

Degenerative disc disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What is myelopathy?

A

Caused by spinal cord compression

  • UMN signs + specific sx depending on where compression is
  • spinal cord disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What is radiculopathy?

A

Caused by spinal root compression

  • LMN signs
  • pain down dermatomes supplied by root
  • weakness in myotome supplied by root
  • no UMN signs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Causes of myelopathy?

A

1) vertebral body neoplasms (secondary malignancy common from: lung, breast, prostate, myeloma)

2) spinal pathology
- disc herniation
- disc prolapse

Rarer causes

  • infection
  • haematoma
  • primary tumour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What is disc herniation?

A

When centre of disc (nucleus populous) has moved out through annulus (outer part) resulting in pressure on nerve root and pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What is disc prolapse?

A

When nucleus populous moves and presses against annulus but doesn’t escape outside annulus. Can produce a bulb in the disc that produces pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Clinical presentation of myelopathy?

A
  • spinal or root pain may precede leg weakness and sensory loss
  • progressive weakness of legs with UMN signs
  • bladder + anal sphincter involvement is LATE –> frequency, hesitancy, later painless retention
  • sensory loss below level of lesion (sensory level)
  • LMN signs at level of lesion
  • UMN signs below level of lesion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Describe S1 nerve root compression?

A

Sciatica

- sensory loss/pain in back of thigh/leg/lateral aspect of little toe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Describe L5 nerve root compression?

A

Sensory loss/pain in lateral thigh, leg and medial side of big toe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Diagnosis of myelopathy?

A

Do not delay imaging (can lead to paraplegia if not decompressed)
*gold standard = MRI (identify site)

130
Q

Tx of mylopathy?

A

If malignant cause = IV dexamethasone to reduce inflammation/oedema
Refer to neurosurgeons
- laminectomy
- microdiscectomy

131
Q

What is cauda equine syndrome?

A

A medical emergency

- spinal damage at or caudal to L1

132
Q

What is the key characteristic in cauda equine syndrome?

A

Flaccid + areflexic weakness

133
Q

Causes of cauda equine syndrome?

A
  • herniation of lumbar disc
  • tumour/mets
  • trauma
  • spondylotisthesis
  • post-op haematoma
134
Q

Clinical presentation of cauda equine syndrome?

A
  • bilateral sciatica
  • saddle anesthesia
  • bladder/bowel dysfunction
  • erectile dysfunction
  • variable leg weakness = flaccid + arreflexic
135
Q

Diagnosis of cauda equine syndrome?

A

MRI to locate lesion

136
Q

Tx of cauda equine syndrome?

A

Refer asap to neurosurgeon:

  • microdiscectomy
  • epidural steroid injection
  • surgical spine fixation
  • spinal fusion
137
Q

What is polyneuropathy?

A
  • disorders of peripheral or cranial nerve, whose distribution is usually symmetrical + widespread
  • often with distal weakening + sensory loss
  • glove + stocking
138
Q

What is a mononeuropathy?

A

Lesions of individual peripheral or cranial nerves

139
Q

Causes of mononeuropathy?

A

Usually local

  • trauma
  • entrapment (tumour)
140
Q

What is mononeuritis multiplex?

A

2 or more peripheral nerves are affected

- happens when causes tend to be systemic

141
Q

What are some causes of mononeuritis multiplex?

A 
Wegener's granulomatosis
Aids/amyloid
Rheumatoid arthritis
Diabetes mellitus
Sarcoidosis

Polyarteritis nodosa
Leprosy
Carcinoma

142
Q

What causes carpel tunnel syndrome?

A

Pressure/compression on median nerve as it passes through carpel tunnel.

143
Q

What is assoc with carpel tunnel syndrome?

A 
Hypothyroidism
Obesity
Diabetes
RA
Pregnancy
Acromegaly
144
Q

Presentation CTS?

A
  • Aching pain in hand/arm
  • Parasthesia in thumb, index, middle, half ring fingers + palm
  • Relived by dangling hand over edge of bed
  • May be sensory loss + weakness of abductor pollicis brevis
145
Q

Diagnosis of CTS?

A

Electromyography shows slowing of conduction velocity

Phallen’s test
Tinel’s test

146
Q

What is phallen’s test?

A

Pt can only maximally flex wrist for 1 minute, causes numbness in CTS

147
Q

What is tinel’s test?

A

Tapping on nerve at wrist causes tingling in CTS pt

148
Q

Tx of CTS?

A

Wrist splint
Steroid injection
Decompression surgery
Behaviour modification

149
Q

what are some poly neuropathies?

A

Motor:
GBS
Lead poisoning
Charcot-Marie Tooth syndrome

Sensory:
Diabetes
Renal failure
Leprosy

150
Q

How do you diagnose polyneuropathies?

A

Hx

Palpable nerve thickening

151
Q

Clinical presentation of polyneuropathy?

A

Sensory

  • numbness (pins + needles) effects extremities first = GLOVE + STOCKING
  • difficulty handling small objects
  • signs of trauma (e.g. burns)

Motor

  • weak/clumsy hands
  • difficulty in walking
  • difficulty in breathing
152
Q

Tx of polyneuropathy?

A

Symptomatic
Pain - amitriptyline or gabapentin
Cramps - quinine
Balance - physio + walking aids

153
Q

What 6 mechanisms can cause nerve malfunction (peripheral neuropathies)?

A

1) demyelination
2) axonal degeneration
3) compression
4) infarction
5) infiltration
6) wallerian degeneration

154
Q

What is MND?

A

Cluster of major degenerative diseases characterised b selective loss of neurones in the motor cortex, cranial nerve nuclei and anterior horn cells.

155
Q

key features of MND?

A
  • destruction of UMN causes both UMN + LMN dysfunction
  • NO SPHINCTER DYSFUNCTION
  • NO SENSORY LOSS
  • NEVER AFFECTS EYE MOVEMENTS
156
Q

What are the 4 main patterns of MND?

A

1) Amyotrophic lateral sclerosis
2) Progressive muscular atrophy
3) Progressive bulbar palsy
4) Primary lateral sclerosis

157
Q

Clinical presentation of MND?

A
  • stumbling spastic gait
  • foot drop
  • weak grip (can’t open jar or door)
  • shoulder abduction difficulty
  • aspiration pneumonia
  • cramps
158
Q

Diagnosis of MND

A

Nerve conduction studies

EMG

159
Q

Tx of MND

A

Antiglutaminergic drugs
- oral riluzole (sodium channel blocker which inhibits glutamine release)

Drooling: amitriptyline

Spasms: oral baclofen

160
Q

What is myasthenia gravis?

A

Autoimmune disease against nicotinic acetylcholine receptors in the neuromuscular junction.

161
Q

RF for myasthenia gravis?

A
  • if under 50 more common in women with pernicious anaemia, SLE, RA, thymic hyperplasia
  • if over 50 more common in men, assoc with thymic atrophy or thymic tumour, RA, SLE
162
Q

What can cause transient myasthenia gravis?

A

D-penicillamine used for treating Wilson’s disease

163
Q

What type of allergy reaction is myasthenia gravis?

A

Type 3
Immune complex deposition
- blocks excitatory effect of ACh

164
Q

Clinical presentation of myasthenia gravis?

A
  • increasing muscular fatigue + weakness
  • muscle groups affected in following order:
    1) extrocular
    2) bulbar
    3) face
    4) neck
    5) trunk
  • look for ptosis, diplopia + mysathenic snarl
  • reflexes may disappear following repetitive activity
165
Q

what tests determine fatiguability in myasthenia gravis?

A

1) Ask patient to count 1-50, as they increase their voice gets less audible
2) Hold finger up high and ask pt to look at it - unable to keep eyes raised

166
Q

What makes myasthenia gravis symptoms worse?

A
  • pregnancy
  • hypokalaemia
  • infection
  • emotion
  • exercise
167
Q

Diagnosis of MG?

A

1) serum anti-AChR antibodies
- raised in 90%
- if negative look for anti-MuSK (muscle specific tyrosine kinase antibodies)

2) EMG + NCS
- Single fibre EMG of orbital muscles shows block and jitter

3) CT thymus
- look for hyperplasia, atrophy or tumour

4) Ptosis improves by >2mm after ice-application to affected eye for 2 mins
5) Tensillon test

168
Q

What is the tensillon test?

A

IV edrophonium (short-acting anti cholinesterase) given and muscle power increases within seconds

169
Q

Tx of MG?

A
  • Symptoms control with anti-cholinesterae (e.g. oral pyridostigmine.)
  • immunosuppression used to treat relapses
    e. g. oral prednisolone
  • thymectomy
170
Q

What are the SE of pyridostigmine

A 
increased salivation
diarrhoea
lacrimation
vomiting
miosis
171
Q

What is myasthenic crisis?

A

Weakness of respiratory muscles during a relapse, can be life treating
- treat with plasmapheresis (antibody removal)
+ IVIG

172
Q

What are some symptoms of cerebellar dysfunction?

A
  • dysarthria
  • dysphagia
  • oscillopsia
  • clumsiness
  • action/intention tremor
  • loss of precision of fine movements
  • nystagmus
  • dysdiadochokinesia
173
Q

What is Huntington’s chorea?

A

A cause of chorea and is a neurodegenerative disorder characterised by the LACK of inhibitory neurotransmitter - GABA.

174
Q

What is chorea?

A

A continuous flow of jerky, semi-purposeful movements, flitting from one part of the body to another.

175
Q

What causes Huntingtons?

A

Mutation on Chr 4 resulting in the repeated expression of CAG sequence
- autosomal dominant with full penetrance

176
Q

Clinical presentation of Huntingtons?

A
  • Prodromal phase of mild psychotic + behavioural symptoms
  • chorea develops
    > can’t sit still, restlessness, lack of coordination
  • dysarthria, dysphagia, abnormal eye movements
  • psychiatric problems
    > behavioural change, aggression, addictive behaviour, depression + anxiety
  • dementia
177
Q

Diagnosis of Huntington’s?

A
  • mainly clinical
  • genetic testing shows many CAG repeats
  • CT/MRI shows caudate nucleus atrophy + increased size of frontal horns of lateral ventricles
178
Q

Tx of Huntington’s?

A
  • chorea: benzodiazepines, sulpiride
  • antidepressants
  • antipsychotics (e.g. haliperidol)
  • aggression: risperidone
179
Q

What is Parkinson’s?

A

Degenerative movement disorder caused by a reduction in dopamine in the substantia nigra

180
Q

What is the triad seen in Parkinson’s?

A

1) rigidity
2) bradykinesia
3) resting tremor

181
Q

RF for Parkinson’s?

A
  • male
  • increasing age
  • family hx
  • non-smoker
182
Q

Clinical presentation of Parkinson’s?

A
  • gradual, slow onset
  • onset is ASYMMETRICAL
  • before motor sx develop:
    > anosmia
    > depression + anxiety
    > aches + pains
    > urinary urgency
    > sleep disorders
  • tremor, rigidity, bradykinesia
183
Q

Describe the tremor in Parkinson’s?

A

worse at rest
asymmetrical
improved by voluntary movements

184
Q

Describe the rigidity in Parkinson’s?

A

increased tone in limbs + trunk

185
Q

Features of bradykinesia?

A 
slow to initiate movement
reduced blink rate
monotonous, hyper phonic speech
micrographic 
expressionless face
186
Q

Describe the gait in Parkinson’s?

A

reduced arm swing
stooped posture
narrow gait
festinance (shuffling gait)

187
Q

diagnosis of Parkinson’s?

A
  • clinical
  • can confirm with response to levodopa
  • MRI may show atrophy
188
Q

what signs present in early Parkinson’s suggest that it is not Parkinson’s?

A
  • dementia (late sign)
  • incontinence
  • symmetry
  • early falls
189
Q

tx for Parkinson’s?

A
  • oral levodopa with decarboxylase inhibitor (co-caroldopa)
190
Q

SE of levodopa?

A

N+V
Psychosis
Jerky movements

191
Q

What is normal pressure hydrocephalus? (NPH)

A

Drainage of CSF is blocked gradually + excess fluid builds up slowly. Enlarged ventricles press on brain and cause symptoms.
- a syndrome of chronic communicating hydrocephalus with normal CSF pressure at LP

192
Q

What are the causes of NPH?

A
  • idiopathic
  • trauma
  • infection
  • SAH
193
Q

What is the triad in NPH?

A

1) gait disturbance - apraxia
2) cognitive impairment
3) urinary incontinence
(wobbly, weird, wee)

194
Q

Ix of NPH?

A
  • CT: enlarged ventricles but normal sulk
  • MRI: no hippocampal volume loss
  • Isotope cisternography
195
Q

Mx of NPH?

196
Q

What is hydrocephalus?

A

an excessive accumulation of CSF within the head caused by a disturbance of formation, flow or absorption.
Causes high pressure and ventricular dilatation.

197
Q

Sx of hydrocephalus?

A
  • headache
  • cognitive impairment
  • ataxia
  • sx of raised ICP
198
Q

Causes of hydrocephalus?

A
  • posterior fossa/brain stem tumours (obstructing aqua duct/4th ventricle outflow)
  • SAH
  • Head injury
  • meningitis (TB)
  • 3rd ventricle cyst
199
Q

How do you treat hydrocephalus?

A

Ventriculoperitoneal shunt

200
Q

What is dementia?

A

A syndrome caused by a number of brain disorders which cause memory loss, difficulties with cognition, problem solving or language as well as difficulties with ADLs

201
Q

causes of dementia?

A

1) alzheimer’s disease
2) vascular dementia
3) lewy body
4) fronto-temporal
5) other: Huntington’s disease, HIV, vitb12/folate deficiency, liver failure, Creutzpelt-Jakob’s

202
Q

what is Alzheimers disease?

A

Degeneration of the cerebral cortex with cortical atrophy.
Neurofibrillary tangles and amyloid plaques.

Most common cause of dementia.

203
Q

what is vascular dementia?

A

Brain damage due to cerebrovascular damage/disease. Can present with signs of vascular pathology (e.g. raised BP, past strokes, focal CNS signs)

204
Q

What sign in the course of dementia points towards vascular dementia?

A

stepwise decline

205
Q

what is lewy-body dementia?

A

deposition of abnormal protein within neurones, presents with fluctuating cognitive impairment and visual hallucinations assoc with Parkinson’s

206
Q

what is pronto-temporal dementia?

A

specific degeneration of frontal/temporal lobes of brain

  • behavioural/personality change
  • lowered inhibition
  • episodic memory loss
207
Q

RF for dementia?

A
  • fam Hx
  • age
  • alcohol
  • obesity
  • high BP
  • hyperlipidaemia
  • diabetes
208
Q

diagnosis of dementia?

A

Hx
Questionnaires (e.g. MMSE)
Exclude treatable causes (e.g. bloods, brain CT if younger)
SPECT scan

209
Q

prevention of dementia?

A
  • healthy behaviours
  • smoking cessation
  • low alcohol
  • physical activity
  • education
210
Q

what medication can be used in dementia?

A

acetylcholinesterase inhibitors

e.g. donepezil

211
Q

what is meningitis?

A

inflammation of the meninges

212
Q

what causes meningitis?

A

Adults + children

  • neisseria meningitidis
  • strep pneumoniae
  • H.influenza

Pregnant women
- listeria monocytogenes

Neonates

  • E.coli
  • group B strep
  • listeria

Immunocompromised

  • CMV
  • TB
  • HIV
213
Q

RF for meningitis?

A
  • intrathecal drub administration
  • immunocompromised
  • elderly
  • pregnant
  • diabetes
  • IVDU
  • overcrowding
214
Q

clinical presentation for meningitis?

A
  • headache
  • neck stiffness
  • fever
  • papilloedema
  • rigors
  • photophobia
  • vomiting
215
Q

diagnosis for meningitis?

A

Blood cultures
LP
CT head
Throat swabs

216
Q

what will CSF of bacterial meningitis show?

A
  • increased polymorphs (neutrophils)
  • raised protein
  • low glucose
217
Q

what will CSF of viral meningitis show?

A
  • increased lymphocytes
  • normal protein
  • normal glucose
218
Q

what will CSF of TB meningitis show?

A
  • increased lymphocytes
  • raised protein
  • low/normal glucose
219
Q

tx for meningitis?

A

Bacterial: IV cefotaxime
Prophylaxis: ciprofloxacin or rifampicin

220
Q

What is encephalitis?

A

Infection and inflammation of brain parenchyma

221
Q

causes of encephalitis?

A
  • mainly viral: HSV 1+2, VZV, EBV

- non viral: bacterial, TB

222
Q

Clinical presentation of encephalitis?

A
  • fever
  • headache
  • altered mental status
  • decreased consciousness
  • behavioural changes
  • focal neurological deficit
223
Q

diagnosis of encephalitis?

A

MRI: inflammation + swelling
EEG: sharp + slow wave complexes
LP: elevated lymphocyte count
Viral detection by CSF PCR

224
Q

Tx of encephalitis?

A

Viral: IV acyclovir

225
Q

What is shingles?

A

Caused by reactivation of VZV in dorsal root ganglia. Development of shingles may indicate a decline in cell-mediated immunity.

226
Q

RF for shingles?

A
  • increasing age
  • immunocompromised
  • HIV
  • Hodgkin’s lymphoma
  • bone marrow transplant
227
Q

clinical presentation of shingles?

A
  • pain + parasthesia in dermatomal distribution
  • malaise, mylagia, fever
  • rash with papules + vesicles in same dermatome
228
Q

Tx for shingles?

A
  • oral acyclovir
  • topical Abx
  • analgesia
229
Q

what is a complication of shingles?

A

post-herpetic neuralgia

  • pain lasting >4months after developing singles
  • burning pain which responds poorly to analgesia
230
Q

how do you treat post-herpetic neuralgia?

A

1) TCA e.g. amitriptyline
2) Anti-epilpetic e.g. oral gabapentin
3) Anti-convulsant e.g. oral carbamazepine

231
Q

What is MS?

A

Chronic auto-immune T-cell mediated inflammatory disorder of CSF in which there are multiple plaques of demyelination in the brain and spinal cord. It occurs sporadically over years.
Disease of CNS with oligodendrocytes targeted.

232
Q

RF for MS?

A
  • female
  • white
  • far from equator
  • exposure to EBV in childhood
  • low levels of sunlight/vit D
233
Q

Where are the plaques in MS?

A

Perivenular

- occur around a vein

234
Q

Why are peripheral nervous system myelinated nerves not targeted in MS?

A

Schwann cells produce this myelin.

235
Q

What are the 3 types of MS?

A

1) relapsing + remitting
2) secondary progressive
3) primary progressive

236
Q

Describe relapsing + remitting MS?

A
  • most common pattern of MS
  • sx occur in attacks (relapses)
  • periods of good health (remission)
  • pt may accumulate disabilities
237
Q

clinical presentation of MS?

A
  • optic neuritis
  • numbness or tingling in limbs
  • leg weakness
  • ataxia
  • spasticity + weakness
  • constipation
  • bladder + sexual dysfunction
238
Q

what is unthoffs phenomenon?

A

symptoms worsen with heat

- e.g. after a bath

239
Q

What is required for diagnosis of MS?

A

2 or more attacks affecting different parts of the CNS.
> 2 lesions disseminated in time and space

MRI + brain scan = diagnostic by showing periventricular lesions

LP: CSF shows oligoclonal IgG bands

240
Q

Tx for MS?

A

Acute
- IV methylprednisolone for <3days

Frequent relapse

  • SC interferon 1B or 1A
  • IV natalizumab
  • dimethyl fumarate

Symptomatic Tx

  • baclofen (for spasticity)
  • catheterisation (urinary Sx)
  • doxazosin (incontinence)
241
Q

What is a coma?

A

State of unrousable unconsciousness.

A coma results in damage to the RAS in brain stem or extensive cortical damage.

242
Q

How do you measure a coma?

A

On the GCS which measures free response to stimuli

1) failure to open eyes in response to verbal command
2) motor response no better than weak flexion
3) incomprehensible verbal sounds in response to pain

243
Q

Causes of a coma?

A

Common:

  • head injury
  • stroke
  • hypoxic ischaemic injury
  • DKA
  • Hypoglycaemia
  • meningitis
  • opiates

Rare:

  • tumour
  • venous sinus occlusion
  • hyperthermia
  • catatonia
244
Q

emergency tx of coma?

A
  • measure GCS
  • emergency resus
  • high flow O2
  • secure IVI access
  • stabilise spine
  • check blood glucose
245
Q

What is status epilepticus?

A

Persistent seizure activity for 30 mins or more
- continuous
- intermittent attacks without recovery of consciousness
Usually a convulsive seizure activity for >10mins

246
Q

Causes of status epilepticus?

A
  • Anti-convulsant withdrawal
  • Alcohol withdrawal
  • Anoxia
  • HTN
  • Cerebrovascular disease
  • Haemorrhage
  • Metabolic disorders
  • Infection
  • Tumour
247
Q

Systemic complications of status epilepticus?

A

Metabolic

  • lactic acidosis
  • hypercapnia
  • hyperglycaemia

Renal

  • acute renal failure from rhabdomyolysis
  • myoglobinuria

Autonomic

  • vomiting
  • incontinence

Cardiac/resp

  • hypoxia
  • arrhythmia
  • aspiration pneumonia
  • cardiac failure
248
Q

Mx of status epilepticus?

A

step 1: ABC, O2, Bloods, ECG, IV access
step 2: lorazepam 4mg IV bolus
step 3: phenytoin 15mg/kg IV diluted
step 4: induce coma with thiopentone

249
Q

What is a brain abscess?

A

Either secondary to a local (ear/sinus) focus OR to a haematogenous spread.

250
Q

Causative organisms of brain abscess?

A
  • staph aureus
  • strep pyogenes
  • gram negatives
  • anaerobes
251
Q

Clinical presentation of brain abscess?

A
  • fever
  • headache
  • focal neurological sx
  • seizures
252
Q

Tx of brain abscess?

A

cefotaxime
flucloxacillin
metranidazole

253
Q

describe NEAD?

A

Non-Epileptic Attack Disorder
Duration: 30mins
Convulsions: non-neuroanatomically accurate. Wild shaking, arms flexing and extending. May be completely still. Wax + wane, pelvic thrusting, eyes closed.

254
Q

what is the recovery like in NEAD?

A

Atypically quick for a prolonged generalised fit. Can be very upset.

255
Q

what is typical PMH for NEAD?

A

Previous unexplained medical symptoms.

Past history of childhood trauma.

256
Q

What is narcalepsy?

A

Sleepiness characterised by irresistible sleep attacks in inappropriate situations (e.g. whilst eating)

257
Q

What is the classical tetrad of narcalepsy?

A

1) sleepiness
2) hypnagogic hallucinations
3) sleep paralysis
4) cataplexy

258
Q

What is cataplexy?

A

Due to sudden loss of muscular tone, falling to the ground or head drop.
Facial twitching may occur.
Episodes last a few seconds but may be as long as 10mins.
- no loss of awareness
- triggers may include emotional outbursts (e.g. laughing)

259
Q

what could cause narcolepsy?

A
  • reduction of hypocretin production from hypothalamus
260
Q

tx of sleepiness?

A
  • modafinil
  • methylphenidate
  • mazindol
261
Q

what is neurofibromatosis 1?

A
  • Autosomal dominant (AD)
  • mutation in NF1 gene, Chr 17q (neurofibromin)
  • clinical phenotype
    > cafe au lait patches, axillary freckling
    > plexiform neuromas
    > optic nerve + brain gliomas
    > pheochromocytoma
262
Q

what is neurofibromatosis 2?

A
  • AD
  • mutation in NF2 gene, Chr 22 (schwanomin)
  • clinical features
    > bilateral acoustic neuromas + meningiomas
263
Q

What is Horner’s Syndrome?

A

Ptosis, meiosis, enopthalmous + anhidrosis due to sympathetic lesion.

264
Q

What is Bell’s palsy?

A

Idiopathic lower motor neurone paralysis of facial nerve.

Inflammation around facial nerve.

265
Q

Sx of Bell’s palsy?

A
  • Weakness of face (usually 1 sided)
  • Drooping of face
  • Drooling
  • Difficulty speaking
266
Q

Tx for Bell’s palsy?

A

Prednisolone to reduce inflammation
Antiviral medication
Eye protection (bc cannot close eye fully)

267
Q

Causes of Bell’s palsy?

268
Q

What is bulbar palsy?

A

Result of diseases affecting lower cranial nerves 7-12

  • speech deficit occurs due to paralysis or weakness of muscles of speech which are supplied by cranial nerves
  • also affects muscles involved in swallowing
269
Q

clinical presentation of bulbar palsy?

A
  • tremulous lips
  • weak tongue
  • drooling (due to dysphagia)
  • dysphonia
  • articulation difficulty
270
Q

what is a cause of progressive bulbar palsy?

271
Q

What infectious diseases can cause bulbar palsy?

A
  • polio

- diphtheria

272
Q

what is radiculopathy?

A

dysfunction of spinal nerve roots

abnormalities: somatosensory, LMN, autonomic

273
Q

what are some symptoms of radiculopathy?

A
  • pins + needles, loss of sensation
  • sharp, radiating pain in neck, arm, demartome of that nerve, may wake at night
  • weakness
  • alternation in tendon reflexes in distribution of a single specific nerve root

> usually unilateral + gradual, may be exacerbated by coughing

274
Q

what nerve roots most commonly affected in radiculogpthy?

A

C6/7 upper

L5/S1 lower

275
Q

what causes anterior cord syndrome?

A

direct anterior cord compression, flexion injuries of the cervical spine, or thrombosis of anterior spinal artery
> leads to variable paralysis below the lesion level with loss of pain + temp perception

276
Q

what causes brown-sequard syndrome?

A
  • hemitransection OR unilateral compression of cord
277
Q

features of brown-sequard syndrome?

A
  • ipsilateral spastic paresis + loss of proprioception + vibration
  • contralateral loss of pain + temp
278
Q

What is the most common cause of vertigo?

A

benign paroxysmal positional vertigo

279
Q

what can cause benign paroxysmal positional vertigo?

A
  • idiopathic (60%)
  • head injury
  • spontaneous degeneration of the labyrinth
  • post-viral neuronitis
  • complication of stapes surgery
280
Q

Symptoms of benign paroxysmal positional vertigo?

A
  • episodes provoked by head movements (rolling over in bed)
  • worse when head is tilted to one side
  • attacks resolved after 20-30seconds
  • brief latent period between movements + attacks (5-20secs)
  • worse in morning
  • nausea

**hearing and tinnitus NOT affected.

281
Q

Ix for benign paroxysmal positional vertigo?

A

Dix-Hallpike test

  • hold patient head, turn to left side then lie them own quickly on their left side. This should trigger nystagmus + vertigo Sx for 20 secs
  • repeat on right side (should be worse on one side)
282
Q

How do you treat benign paroxysmal positional vertigo?

A

Epley’s manoeuvre
- aim is to reposition otoliths back into the utricles from the posterior semicircular canals so there should be no nystagmus.

283
Q

What can cause vertebral pain syndrome?

A
  • usually wear and tear
  • TB
  • bacterial discitis
  • osteomyelitis
  • osteoporotic fractures
  • metastatic disease
284
Q

Symptoms of vertebral pain syndrome?

A
  • aching pain (doesn’t radiate)
  • back stiffness (worse with movement)
  • paravertebral muscle spasms + tenderness
  • restricted ROM
285
Q

Red flags for back pain?

A
  • recent violent trauma or minor trauma if osteoporotic <20yrs or >50yrs at new onset
  • Hx of cancer
  • steroids
  • HIV/immunosuppression
  • fever, chills, weight loss
  • recent bacterial infection
  • neurological deficit in Lowe limbs
  • structural deformity pain = constant, severe, progressive, without relief with rest
  • morning stiffness
286
Q

What is spinal claudication?

A

AKA neurogenic claudication

  • bilateral radiating leg pain/paraesthesia which comes on with walking
  • relieved by rest or bending forwards

Symptom of lumbar spinal stenosis; ischaemia of the lumbar nerve roots (type of radiculopathy)

287
Q

What is transverse myelitis?

A

Acute inflammatory disorder of spinal cord over days, usually after viral infection (can be from SLE, sarcoidosis, infection, MS)

288
Q

Sx of transverse myelitis?

A
  • weakness
  • numbness of limbs
  • pins + needles
  • bladder/bowel dysfunction
289
Q

Ix and Tx of transverse myelitis?

A

Ix: MRI
Tx: high dose steroids + Abx if infection

290
Q

What is subacute combined degeneration of the cord?

A

Peripheral + cord (combined) nerve damage.

291
Q

Sx of subacute combined degeneration of the cord?

A
  • numbness/tingling of fingers/toes
  • distal sensory loss
  • absent ankle jerks
  • exaggerate knee jerks
  • upgoing plantar reflexes

Later Sx

  • optic atrophy
  • retinal haemorrhage
  • sphincter disturbance
  • severe generalised weakness
  • dementia
292
Q

What is spinal stenosis?

A

Narrowing of spinal canal or neural foramina producing root ischaemia and neurogenic claudication.

293
Q

Ix of spinal stenosis?

A

Lumbar spine xray

Lumbar spine MRI

294
Q

Tx of spinal stenosis?

295
Q

C5 myotome

A

shoulder abduction

bicep jerk

296
Q

C6 myotome

A

elbow flexion

supinator jerk

297
Q

C7 myotome

A

elbow extension

triceps jerk

298
Q

L3/L4 myotome

A

knee extension

knee jerk

299
Q

L5 myotome

A

ankle dorsiflexion (upwards)

300
Q

S1 myotome

A

ankle plantar flexion (downwards)

ankle jerk

301
Q

C4 dermatome

302
Q

T4 dermatome

303
Q

T1 dermatome

A

medial arm

304
Q

T10 dermatome

305
Q

L2/L3 dermatome

A

anterior + inner leg

306
Q

L4 dermatome

307
Q

L5/S1/S2 dermatome

A

posterior + outer leg

308
Q

S4 dermatome

A

perianal area

309
Q

what is wernicke korsakoff syndrome?

A

spectrum of disease resulting from thiamine deficiency, usually related to alcohol abuse

310
Q

presentation or wernicke Korsakoff syndrome?

A
  • vision changes
  • loss of muscle coordination
  • loss of memory
  • inability to form new memories
  • hallucinations
  • confabulation
  • retrograde amnesia
311
Q

Tx of wernicke Korsakoff syndrome?

A

Oral thiamine

Multivitamins

312
Q

What is steroid myopathy?

A

Steroids can cause atrophy of muscle fibers, leading to muscle weakness.
S/e of steroid use

313
Q

What are inflammatory myopathies?

A

Disease featuring weakness and inflammation of msucles and muscle pain.

314
Q

Classes of inflammatory myopathies?

A
  • Polymyositis
  • Dermatomyositis
  • Inclusion-body myositis
315
Q

What enzyme is raised in polymyositis?

A

Creatine Kinase

316
Q

What do Gottrons papules indicate?

A

Dermatomyositis

317
Q

Describe myotonic myopathy

A

Progressive muscle wasying and weakness. OFten have prolonged muscle contractions (myotonia) and are not able to relax muscles after use (eg releasing door handle)

318
Q

What is Muscular Dystrophy?

A

Inherited gentic disorder causing muscle weakness.

319
Q

Symptoms of muscular dystrophy?

A
  • weakness
  • delay in milestones in kids
  • wasting
  • hypertrophy of muscles
  • aches/pains
320
Q

Diagnosis of muscular dystrophy?

A
  • Creatine kinase
  • Biopsy
  • Genetic analysis
    EMG
  • Muscle ultrasound
321
Q

Treatment of MD?

A
  • physio

- steroid tx

322
Q

What ae symtpoms of statin myopathy?

A

Cramps
Heaviness
Stiffness

3a (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions