Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 4 Additional Notes > Neurology > Flashcards

Neurology Flashcards

1
Q

Investigations for suspected GBS

A

Lumbar puncture (cytoalbuminologic dissociation- raised protein without raised WCC) and nerve conduction studies (decreased motor nerve conduction)

Also check (for any limb weakness)- FBC, UE, LFT, CRP, ESR, bone profile (calcium), phosphate, magnesium, B12, folate (haemanitics)

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

Myasthenia gravis

A

Autoimmune disorder, resulting in antibodies to acetylcholine receptors

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

Myasthenia gravis features

A

Muscle fatigability- muscles become weaker during periods of activity and improve after rest
Diplopia and ptosis (eg, at the end of the day after watching TV and reading)
Weakness of face, neck, limb girdle muscles
Dysphagia and slowness in chewing food
NO SENSORY PROBLEMS

NB- if concurrent thymoma, may see SVC syndrome (distended neck veins)

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

Myasthenia gravis associations

A

Thymoma
Autoimmune disorders eg. SLE
Thymic hyperplasia (most common)

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

Investigations for MG

A

All the blood tests you would do for limb weakness
Electromyography- diminished response to repetitive stimulation on EMG
Acetylcholine receptor auto antibodies (or anti muscle specific tyrosine kinase antibodies)
CT thorax to exclude thymoma
Creative kinase is normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Long term management of MG

A

Pyridostigmine
Prednisolone
Immunosuppressants eg. Azathioprine

NB- thymectomy in hyperplasia but not thymoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Management of acute MG crisis

A

Plasmapheresis
IV immunoglobulins

NB- resp failure can develop and kill these patients. Be prepared to step up management early

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

Drugs that can exacerbate pre existing MG

A

Beta blockers
Lithium
Phenytoin
Antibiotics eg. Gentamicin, macrolide, tetracyclines
Penicilliamine
Quinidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Myelopathy

A

Disorders due to compression of the spinal cord

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

Myelitis

A

Neurological disorder due to inflammation of the spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Causes/risk factors for myelopathy

A

Trauma
Infection (abscess)
Neoplasm
Degenerative disease eg. Spinal stenosis, ankylosing spondylitis, disc prolapse
High axial loading job and smoking (disc prolapse risk factors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Features of myelopathy

A

Limbs affects (upper or lower) depends on the site of the lesion eg. Cervical or thoracic region. Usually bilateral

Pain
UMN signs (increased tone, spasticity, hyperreflexia, up going plantar reflex, weakness)
Loss of motor function
Impaired sensation eg. Numbness, ataxia, loss of proprioception or vibration sense
Impaired bladder and bowel control (Impotence too)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Features of myelitis

A

Same as myelopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Lumbar region and myelopathy

A

No spinal cord in lumbar region, just nerve roots, so won’t get UMN lesions when a lumbar disc herniates (but can get LMN signs eg. Cauda equine, get autonomic (bladder and bowel), sensory (parathesia), and LMN signs (absent reflexes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Radiculopathy

A

Neurological disease due to compression of nerve roots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Features of cauda equine syndrome

A

Back pain, radicular pain
Neurological deficits below the lesion eg. Sensory abnormalities first, then motor abnormalities
Bladder, bowel, sexual dysfunction
Saddle parasthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

General features of myosotis (PM or DM)

A

Bilateral proximal muscle weakness (pelvis and shoulder girdle)
Functional difficulties eg. Dressing, climbing stairs
Dysphagia
Muscle tenderness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cutaneous features of dermatomyositis

A

Gottrons papules (rough red papules over the extensor surfaces of the fingers)
Mechanics hands- thickening and hyperpigmentation
Heliotrope rash (upper eyelids)
Midfacial erythema (affects nasolabial folds unlike SLE)
Photosensitive rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Inclusion body myosotis features

A

Progresses slowly over many years
Same symptoms as general myosotis but affects proximal and distal muscle groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Investigations for suspected myosotis

A

Neurological examination and observations
FBC UE other electrolytes
CK- raised
Antibodies
Muscle biopsy
MRI- malignancy

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

Difference between PM, DM, and IBM

A

PM and DM are associated with younger people and malignancy, they can present quickly, affect the proximal muscles

IBM progresses slowly over many years and is associated with the elderly, affects the proximal and distal muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Antibodies for myosotis

A

PM- anti jo 1
DM- anti Mi 2 & ANA & anti synthase & anti jo 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Management of myosotis

A

Refer to rheumatology
Supportive measures NSAIDS etc
Treat underlying malignancy
Steroids
Immunoglobulins
Biologics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Differentiate an acute peripheral neuropathy and an acute myelopathy (LMN vs UMN)

A

Tone and reflexes
Facial involvement

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

Facial nerve palsy features

A

Changes to muscles of facial expression eg. Inability to smile etc.
Hyperacusis or hearing changes
Reduced taste sensation
Reduced tears and saliva (dry mouth and eyes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Causes of unilateral facial palsy

A

Bell’s palsy (pregnancy is a risk factor for Bell’s)
Ramsay hunt syndrome
Acoustic neuroma/ cholesteatoma
Parotid tumours
HIV
DM
Malignant otitis externa
Facial trauma

Stroke, MS, tumour (UMN lesion- forehead is spared)

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

Causes of a bilateral facial nerve palsy

A

Sarcoidosis
GBS
Lyme disease
Bilateral acoustic neuromas
Bell’s palsy
MND (UMN or LMN)

NB- these can cause unilateral palsies too

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

When to give steroids in Bell’s palsy

A

Within 72 hours of onset
NB- if it hasn’t resolved within 3 weeks- refer to ENT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is shingles

A

Herpes zoster infection, caused by reactivation of the varicella zoster virus (chicken pox)- it had remained dormant in the dorsal root of cranial nerve ganglia for many years before reactivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Features of shingles (herpes zoster infection)

A

Prodrome period- burning pain over the dermatome (severe pain), fever, headache, lethargy

Rash- vesicular, macular rash over the affected dermatome, well demarcated and doesn’t cross the midline

NB- diagnosis is clinical

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

Management of shingles (herpes zoster infection)

A

Patients are infectious- need to avoid pregnant women and the immunocompromised (wait until vesicles have crusted over- 7 days after onset), cover lesions to reduce risk of spread
Analgesia (paracetamol and NSAIDs, then amitriptyline)
Antivirals within 72 hours eg. Aciclovir (reduces incidence of post heretic neuralgia)

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

Complications of shingles (herpes zoster infection)

A

Post herpetic neuralgia (resolves in 6 months)
Herpes zoster ophthalmicus
Herpes zoster oticus/Ramsay hunt syndrome- ear lesions and facial paralysis

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

Brocas (expressive) dysphasia

A

Non fluent speech (content preserved but delivered in a very laboured/halting way)
Repetition is impaired
Comprehension in tact

Inferior frontal gyrus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Global aphasia

A

Non fluent speech
Comprehension impaired (receptive and expressive dysphasia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Wernickes aphasia (receptive aphasia)

A

Fluent speech, but sentences make no sense, there is word substitution and neologisms
Comprehension impaired

Superior temporal gyrus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Conduction aphasia

A

Fluent speech
Compression intact
Inability to repeat words and phrases, aware of mistakes they make

Arcuate fasiculus - the connection between Wernicke’s and Broca’s area

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

Features of an Arnold chiari malformation

A

Headache
Non communicating hydrocephalus
Syringomelia (CSF in the spinal cord)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is autonomic dysreflexia

A

Clinical syndrome that occurs in people who have a spinal cord injury at or above T6

Triggered by faecal impaction or urinary retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Features of autonomic dysreflexia

A

Extreme HTN, flushing and sweating at the level above the lesion, severe cases haemorrhagic stroke

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

Management of autonomic dysreflexia

A

Control precipitating stimulus
Treat life threatening HTN and or bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Causes of a brain abscess

A

Extension of sepsis from middle ear or sinus, trauma, surgery, penetrating head injuries, embolic events from endocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Features of a brain abscess

A

Headache, fever, focal neurology, other features of raised ICP eg. Nausea, papilloedema, seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Antibiotic choice for a brain abscess

A

IV 3rd generation cephalosporin and metronidazole

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

What is the most common brain tumour

A

Metastatic brain cancer

Lung (most common) breast bowel skin kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Where do meningiomas arise from

A

Dura mater

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Vestibular schwannoma

A

Previously called acoustic neuroma
Benign tumour arising from the 8th cranial nerve
Unilateral hearing loss, facial nerve palsy, tinnitus, vertigo, absent corneal reflex
Neurofibromatosis type 2- bilateral vestibular schwannomas
MRI cerebellopontine angle (galladium enhanced)

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

Brown sequard syndrome

A

Caused by LATERAL hemi section of the spinal cord

Ipsilateral weakness below the lesion
Ipsilateral loss of proprioception and vibration sensation
Contralateral loss of pain and temperature sensation

NB- think pain and temp are the worst so you would want them on the other side

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

Cerebellar syndrome causes

A

Unilateral lesions cause Ipsilateral signs

P - Posterior fossa tumour
A - Alcohol
S - Multiple sclerosis
T - Trauma
R - Rare causes
I - Inherited (e.g. Friedreich’s ataxia)
E - Epilepsy treatments eg. phenytoin
S - Stroke

NB- vermis= ataxia, hemisphere= finger to nose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Features of cerebellar syndrome

A

DANISH

Dysdiadochokinesia, dysmetria (past pointing)
Ataxia
Nystagmus
Intention tremor
Slurred staccato speech, scanning dysarthria
Hypotonia

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

Features of a common peroneal nerve injury

A

Foot drop
Weakness of foot dorsiflexion
Weakness of foot eversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Features of Creutzfeldt-Jakob disease

A

Rapid onset dementia
Myoclonus

NB- comes from BSE (mad cow disease)

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

Drugs that can cause peripheral neuropathy

A

Amiodarone
Metronidazole
Nitrofurantoin
Isoniazid
Vincristine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Syncope and DVLA

A

Simple faint- no restriction
Single episode, explained and treated- 4 weeks
Single episode, unexplained- 6 months
2 or more- 12 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Traumatic brain injury and the DVLA

A

6 months stop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Stroke or TIA and the DVLA

A

1 month (if no residual defecits, don’t need to tell DVLA)

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

Multiple TIAs over short time

A

3 months off and tell DVLA

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

Craniotomy and the DVLA

A

1 year off if meningioma, 6 months off if pituitary tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Trans sphenoid all surgery and the DVLA

A

Can drive when no residual symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Narcolepsy and the DVLA

A

Cease driving on diagnosis, restart when control of symptoms

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

Chronic neurological disorders and the DVLA

A

Tell DVLA, carry on driving, they may assess you regularly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Investigations for encephalitis

A

Lumbar puncture (lymphocytosis, elevated protein) with MCS
PCR for HSV (from CSF)
MRI head

NB- LP gold standard (MRI only shows temporal changes in HSV associated disease)

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

Management of encephalitis

A

IV aciclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Extradural (epidural) haematoma

A

Middle meningeal artery
Lucid interval
Biconvex/lentiform collection (limited to suture lines)

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

Causes of foot drop

A

Common peroneal nerve lesion
Sciatic nerve lesion
UMN lesion eg. Stroke

NB- avoid kneeling, crossing legs, should heal in several months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Raised ICP headache

A

Triggered by cough, vaslsalva manoeuvres, sneeze, exercise, worse in morning

Visual disturbance and focal neurology may be present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Huntingtons disease

A

Autosomal dominant
Trinucleotide repeat of CAG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Features of HD

A

Chorea
Personality change
Intellectual impairment
Dystonia
Saccades

NB- management- SALT, end-of-life planning, genetic counselling, benzo’s/ AP’s (reduce movements)

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

Idiopathic intracranial HTN features

A

Headache, blurred vision, papilloedema, enlarged blind spot, sixth nerve palsy, pulsatile tinnitus

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

Risks for IIH

A

Obese, female sex, pregnancy, combined OCP (not progesterone only) steroids, tetracyclines (lymecyclime for acne, doxycycline), vitamin A and lithium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Features of an intracranial venous thrombosis

A

Headache (thunderclap, sudden onset)
Nausea and vomiting
Seizures, hemiplegia, cranial nerve palsies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Amyotrophic lateral sclerosis

A

Most common MND
LMN signs in arms and UMN signs in legs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Primary lateral sclerosis

A

UMN signs only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Progressive muscular atrophy

A

LMN signs only
Distal muscles before proximal
Best prognosis

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

Progressive bulbar palsy

A

Palsy of tongue, muscles or chewing and swallowing, and facial muscles due to loss of function of brain stem motor nuclei
Worst prognosis

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

General features of MND

A

Fasiculations
Absence of sensory signs and symptoms
Mixed UMN and LMN signs in ALS
Wasting of small hand muscles and tibial is anterior is common
Hypophonic speech
Dysphagia- liquids first then solids
Doesn’t affect external eye muscles
No cerebellar involvement
Abdominal reflexes preserved, sphincter dysfunction if present is a very late feature

Associated with FTD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Investigations for MND

A

Clinical diagnosis
Blood tests for electrolytes etc.
Normal motor condition on nerve conduction studies
EMG (different to nerve conduction)- see muscles that have lost nerve supply
MRI- exclude myelopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Management of MND

A

Supportive- exercise, diet, physio etc.
Medical- riluzole (ALS- 3 months)
Respiratory support- BIPAP at night

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Pituitary apoplexy

A

Sudden enlargement of a pituitary tumour secondary to haemorrhage or infection

Sx- headache (thunderclap), neck stiffness, visual field defects, cranial nerve palsies, signs of pituitary insufficiency;

low ACTH
tiredness
postural hypotension

low FSH/LH
amenorrhoea
infertility
loss of libido

low TSH
feeling cold
constipation

low GH
if occurs during childhood then short stature

low prolactin
problems with lactation

Management- steroid replacement (and replacement of other pituitary hormones), fluid balance, surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Features of raised ICP

A

Headache, vomiting, reduced consciousness, paipilloedmea, cushings triad (wide pulse pressure (HTN), bradycardia, irregular (reduced) breathing)

This is in contrast to shock- decreased BP, tachycardia, and tachypnoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Management of raised ICP

A

Treat underlying cause
Head elevation to 30 degrees
IV mannitol
Controlled hyperventilation (reduce pCO2)
Remove CSF eg. Shunt

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

Causes and associations of restless leg syndrome

A

Family history
Iron deficiency anaemia
Uraemia
DM
PD
Pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Management

A

Exercises eg, stretches, walking
Treat iron deficiency
Dopamine agonists eg. Ropinirole or pramipexole
Benzodiazapenes
Gabapentin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Subacute combined degeneration of the spinal cord

A

Vitamin B12 deficiency
Dorsal columns and lateral corticospinal tracts affected
Joint position and vibration sense lost first, then distal parasthesia
UMN signs in legs
If untreated permanent damage can persist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Von hippel lindau syndrome

A

Autosomal dominant predisposing to neoplasia

Cerebellar haemangiomas
Retinal “”
Renal cysts
Phaeochromocytoma
Renal carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Warning features in GBS

A

Autonomic dysfunction eg. Tachycardia

Respiratory muscle weakness- dyspnoea (need serial FVC measurements), if dropping, transfer to ICU)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Transverse myelitis and MS

A

Oligoclonal bands in CSF can suggest transverse myelitis or MS (they suggest inflammation of the spine and resulting myelopathy). If first presentation you could suggest TM, but if previous neurological symptoms then you would think MS (history is important here).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Causes of a raised CK

A

Myosotis eg. PM or DM
Rhabdomyolysis (post trauma or prolonged stay on floor)
AKI
MI
Statins
Strenuous exercise

NB- not PMR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Viral meningitis or encephalitis based on CSF interpretation

A

If CSF is thought to be contained with a virus, whether it is meningitis or encephalitis depends not only on imaging, but also clinical history and picture (encephalitis patients more sick- they may have focal neurology, behavioural changes, seizures etc.)

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

Delirium following herpes zoster infection

A

Think herpes zoster encephalitis?

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

Management of any mononeuropathy eg. Common peroneal nerve palsy

A

Supportive- avoid compressing it, avoid contact sports, splint, physio etc.
Medical- analgesia if pain (usually there isn’t)
Surgical- nerve repair if not healed and causing issues months down the line

91
Q

Difference between a common peroneal nerve palsy and prolapsed IV disc

A

Prolapsed disc- significant pain and loss of Ipsilateral ankle reflex

Common Peroneal nerve palsy- typically painless and ankle reflex is preserved (L5 Radiculopathy)

92
Q

Cause of wrist drop

A

Compression of radial nerve
Saturday night palsy

93
Q

Relapsing remitting MS

A

Most common
Acute attacks last 1-2 months, followed by periods of remission

94
Q

Secondary progressive MS

A

Relapsing remitting patients who have deteriorated and developed neurological signs and symptoms between relapses
Develops in 65% of RR patients within 15 years of diagnosis

95
Q

Primary progressive MS

A

Progressive deterioration from onset

96
Q

Diagnosing MS

A

2 or more relapses and either objective or clinical evidence of 2 or more lesions (disseminated in time and space)

NB- MRI of head and spine will show lesions, lumbar puncture (oligoclonal bands) will also aid diagnosis

Also do neuro exam, FBC, UE, LFT, TFT, B12, folate

97
Q

Features of MS

A

Visual- optic neuritis (RAPD can be a sign of current or old optic neuritis- swinging light test, damage to CN II), optic atrophy, Uhtoffs phonomenon (worsening of Sx following increased temperature), INO (conjugate gaze palsy)

Sensory- parastehsia, pins and needles, trigeminal neuralgia, Lhermittes syndrome (neck flexion)

Motor- increased tone and spasticity (depends on where lesions are eg. Spinal cord lesion could cause spastic paraparesis)

Cerebellar- ataxia, tremor, other cerebellar syndromes

Others- urinary incontinence, sexual dysfunction, intellectual deterioration

98
Q

Management of Acute MS relapse

A

High dose steroids (oral or IV methylprednisolone) for 5 days to shorten the length of an acute relapse

99
Q

General management of MS

A

Supportive- physiotherapy, lifestyle modifications, patient education, spasticity (baclofen and gabapentin), treat bladder and bowel dysfunction (bladder scan first to assess bladder emptying) eg. Catheter or stoma or oxybutinin (urinary frequency), occupational therapy, fatigue (amantidine)
Medical- natalizumab , a monoclonal antibody is better than beta interferon

100
Q

Most common presenting symptom of MS

A

Fatigue

101
Q

Febrile convulsions

A

Typically children between 6 months- 5 years old
Generalised tonic clinic in nature

102
Q

Alcohol withdrawal seizures

A

Sudden stopping of alcohol in a patient with alcohol excess history
Peak-36 hours

103
Q

Psychogenic non epileptic seizures

A

Epileptic like seizures but no electrical discharges
May have history of mental health problems or a personality disorder

104
Q

Infantile spasms (West syndrome)

A

Flexion of head trunk and limbs
Progressive mental handicap
EEG- hypsarrhytmia
Usually secondary to a serious neurological abnormality

NB- may progress to Lennox gaustaut syndrome (atypical absences, falls, jerks etc).

105
Q

Benign Rolandic epilepsy

A

Parastehsia (unilaterl face), usually on waking up

106
Q

Juvenile myoclonic epilepsy (Janz syndrome)

A

Onset in teens (girls)
Generalised seizures, often in morning
Daytime absences
Sudden muscle jerks (eg. dropping things)
Good response to valproate

NB- like absence seizure epilepsy, but muscle jerks (typically in morning)

107
Q

Pharmacological management of epilepsy

A

AED started after second seizure
Generalised seizures- sodium valproate (lamotrigine or carbamazepine 2nd line)
Focal seizures- carbamazepine/lamotrigine (valproate 2nd line)

NB- always prescribe by brand

108
Q

Adverse effects of valproate

A

Increase appetite and weight gain
Alopecia
P450 enzyme inhibitor
Ataxia
Tremor
Hepatitis
Pancreatitis
Teratogenic
Thrombocytopenia

109
Q

Adverse effects carbamazepine

A

AGRANULOCYTOSIS- sore throat
P450 enzyme inducer
Dizziness and ataxia
Drowsiness
SIADH
Visual disturbances
Aplastic anaemia

110
Q

Adverse effects lamotrigine

A

Stevens johnson syndrome

111
Q

Adverse effects phenytoin

A

P450 enzyme inducer
Dizziness and ataxia
Drowsiness
Peripheral neuropathy
Megaloblastic anaemia
Teratogenic

112
Q

Localising lesions of focal seizures

A

Temporal lobe (head)- hallucinations, epigastric rising, emotion, lip smacking, grabbing, or plucking, dysphagia, deja vu

Frontal lobe (motor)- head of leg movements, posturing, post ictal weakness, Jacksonian march (can get secondary tonic-clonic seizure after initial Jacksonian march)

Parietal lobe (sensory)- parasthesia

Occipital lobe (visual)- floaters or flashes

113
Q

When to investigate for epilepsy

A

After the second generalised seizure eg. EEG and MRI brain

114
Q

Management of a first seizure/ suspected epilepsy

A

Refer to neurology/ first seizure clinic (don’t drive, bring the witness with you if possible)
Lifestyle NA agent- promote general health
Inform the DVLA
Advice eg. Shower, swimming, heights, traffic, cautious with heavy hot or electrical equipment
Adhere to AED’s
Surgery for extreme cases

115
Q

Status epilepticus

A

Single seizure lasting longer than 5 minutes

Or

More than 2 seizures in a 5 minute period without the patient returning to normal between them

116
Q

Management of status epilepticus

A

ABCDE (check oxygen and BM)
In community- 10mg diazepam rectally or 10mg buccal midazolam
In hospital- secure airway, IV lorazepam 4mg (repeated after 10 minutes)
If ongoing status- start a phenytoin (2nd line agents) infusion (phenobarbital if already on phenytoin)
If refractory, after 45 minutes induce general anaesthesia (thiopental sodium)

117
Q

What to do when someone has a seizure in the community

A

Put patient in safe position eg, lay on floor (recovery position if possible)
Put something soft under head
Remove obstacles that could cause injury
Make a note of time it started
Call ambulance if longer than 5 minutes- or if this is first seizure

118
Q

Spastic tetraparesis

A

UMN signs in all 4 limbs

119
Q

Spastic paraparesis

A

UMN signs in 2 limbs

120
Q

Cranial nerve and limb involvement

A

Either stroke or brain stem pathology

121
Q

Causes of recurrent stroke in a young person

A

Thrombophilia
Emboli (infective endocarditis)
Vasculitides
Autoimmune condition (SLE)
Recurrent drug use (cocaine);

122
Q

Coughing and headaches

A

The red flag is when the headache is precipitated by the cough (raised ICP), not made worse (migraine)

123
Q

Causes of increased ICP with a normal head CT

A

Cerebral venous sinus thrombosis
Idiopathic intracranial hypertension

NB- need to do a CT venogram to exclude the VST first

124
Q

Signs of MG

A

Fatiguable ptosis- keep eyes in vertical gaze and eyelids will shut
Weak orbital muscles- shut eyes and they should be easy to open
Inability to whistle

125
Q

Measuring neuromuscular respiratory impairment

A

FVC (restrictive disease- peak flow is used for obstructive disease such as COPD and asthma)

Breath count is a surrogate marker eg. Take breath and count as many numbers as possible

Neck flexion weakness is a bad sign in GBS (C345 supply diaphragm but also control neck flexion, if this is weak, diaphragm may also be weak)

126
Q

Metabolic causes of encephalopathy

A

Hypoxia, increased urea,increased ammonia, septic encephalopathy (delirium), blood sugars

127
Q

Red flags for headache

A

Worse when leaning forward, coughing
Wakes patient up at night
Morning headache
Associated neurological and visual deficits
Signs of infection eg. Meningism (photophobia)

128
Q

Causes of a thunderclap headache

A

SAH
Intracerebral bleed
Dissected vertebral or carotid arteries
Cerebral venous sinus thrombosis (previous malignancy, young, female, OCP, thrombophilia, dehydration are risk factors)
Low CSF pressure (meningeal rupture)- headache worse standing up (not lying down)

NB- thunderclap headache is immediate. If it builds up over 30-40 minutes it isn’t a thunderclap headache.

129
Q

Incontinence and UMN lesions

A

Lower spinal lesion- lack of sensation (don’t feel urge to go). Insensate

Upper spinal lesion- urgency incontinence

130
Q

Hyper intensities

A

Lesions in demylinating conditions eg. MS

131
Q

Hemiplegic gait

A

Unilateral flexed upper limb and extended lower limb (elongated)
Patients circumduct affected leg

UMN

Causes- stroke, SOL, trauma, MS

132
Q

Diplegic (scissor) gait

A

Similar to hemiplegic gait but bilateral in nature
Circumduction of both legs and potential overlap

UMN

Causes- prolapsed disc, spinal tumour or infarct, spastic paraparesis, cerebral palsy, MS, MND (lower motor neurone signs)

133
Q

Parkinsonism gait

A

Slow to start walking
Reduced stride length with short steps. Subsequent steps may get smaller (festinant)
Reduced arm swing
Stooped posture
Resting tremor
Impaired balance or hesitancy on turning

Causes- IPD or Parkinson plus syndromes

134
Q

Ataxic gait

A

Cerebellar, sensory, or vestibular cause

Stance- broad based
Stability- staggering, slow, unsteady (if a unilateral cerebellar lesion- will veer towards side of lesion)
May require a walker/something to hold onto whilst walking
Turning- turning manoeuvre can be difficult

May be additional Sx;

135
Q

Features associated with cerebellar ataxia

A

DANISH

Dysdiadokokinesia
Ataxia
Nystagmus
Intention tremor
Speech
Hypotonia

Causes- cerebellar stroke, SOL, MS, alcoholism, B12 deficiency, lithium, spinocerebellar ataxia

136
Q

Features associated with sensory ataxia

A

Positive Rhombergs (cerebellar ataxia- unsteady whether eyes open or closed, sensory, more prominent when eyes closed)
Impaired proprioception
Impaired vibration sense
Absent cerebellar signs

Cause- peripheral neuropathy eg. DM

137
Q

Features associated with vestibular ataxia

A

Vertigo
Nausea
Vomiting

Causes- labyrinthitis, Ménière’s disease, acoustic neuroma

138
Q

Neuropathic (high-steppage) gait

A

Foot drop and toe dragging- to prevent this there is excessive knee and hip flexion (high steppage)

LMN

Causes- common nerve palsy, L5 radiculopathy (disc), MND

139
Q

Myopathic (waddling or trendelenburg) gait

A

Waddling from side to side
Circumduction of legs
Positive Trendelenburgs sign- stand on one leg, pelvis drops to contra lateral side (due to weakness of abductor muscles on other side)

Cause- thyroid disease, Cushing’s syndrome, acromegaly, poly myalgia rheumatica, polymyositis, muscular dystrophy (Duchenne)

140
Q

Choreiform (hyperkinetic) gait

A

Involuntary movements during gait eg. Oreo facial dyskinesia
Chorea in upper and lower limbs

Causes- HD, Sydenham’s chorea, cerebral palsy, Parkinson’s medications, Wilson’s disease

141
Q

Antalgic gait

A

Stance phase reduced on affected leg giving limp appearance

Cause- OA, fracture, nerve entrapment eg. Sciatica

142
Q

Cancer patient with meningism

A

Think malignant meningitis

143
Q

Causes of Horners syndrome’

A

Brain stem, lung, or carotid pathologies (BLC)

Brain stem tumour, Pam coast lung tumour, carotid artery dissection or aneurysm, migraine (but if new onset in an older person- be suspicious and do a CT angiogram)

144
Q

When do signs of a stroke typically appear on a CT

A

12 hours afterwards

145
Q

Phenytoin adverse effects

A

Can cause heart block and arrhythmias
With any heart disease (structural or arrhythmia (AF)) don’t use IV phenytoin

146
Q

What anaesthetic agent are people with MG resistant to?

A

Suxamethonium

147
Q

Cranial nerves affected in vestibular schawannomas

A

V VII VIII

148
Q

When to intubate somebody

A

If GCS is less than 8

149
Q

What is the mechanism of reducing ICP with hyperventilation

A

Reduced blood CO2 to induce cerebral vasoconstriction

150
Q

Acute vs chronic subdural haematoma

A

Acute- hyper dense (bright)

Chronic- hypodense (dark)

151
Q

Criteria for brain stem death

A

Deep coma of known aetiology
Reversible causes excluded
No sedation
Normal electrolytes

152
Q

Management of hydrocephalus

A

EVD- acute
VPS- long term therapy
Obstructive (non-communicating)- remove obstructive pathology

NB- never use LP in obstructive hydrocephalus or reduced ICP as the difference in cranial and spinal pressures induced by the drainage will cause brain herniation

153
Q

What ECG change may be seen during SAH

A

ST elevation

154
Q

Management of SAH

A

Coil (but some need clipping via a craniotomy)
Vasospasm prevented by nimodipine (calcium channel antagonist) for 21 days

NB- hyponatraemia due to SIADH may occur

155
Q

What are the 2 most important tests to do before any others when someone presents with a seizure

A

Blood glucose
Oxygen (ABG, sats)

156
Q

Syringomelia

A

Fluid filled cyst in the centre of the spinal cord (anterior white commissure)

Associations- Arnold chiari malformation, trauma, tumours, idiopathic

Cape like loss of pain and temperature sensation (think shoulders)- spinothalamic tracks in anterior commissure damaged
Spastic weakness (lower limbs)
Neuropathic pain
Upgoing plantars
Autonomic features
Horner’s
Scoliosis (if chronic and untreated)

Brain and spine MRI- exclude tumour, tethered cord, chiari malformation
Can have a shunt

157
Q

Co careldopa

A

Can only be given orally
If someone can’t take their usual levodopa, give a dopamine agonist patch

158
Q

Stopping an AED

A

If seizure free for 2 years, done over 2-3 months

159
Q

Central contusions on scan but no focal neurology

A

Insert an intra cranial pressure monitoring device
May develop raised ICP in a few days

160
Q

EEG for absence seizures

A

3Hz oscillations

161
Q

Tuberous sclerosis

A

Depigmented ash leaf spots which fluoresce under UV light
Roughened patches of skin over lumbar spine
Angiofibromas
Fibromatas beneath nails
Cafe au lait spots
Developmental delay
Epilepsy
Retinal haematomas

162
Q

Hoffman sign

A

UMN lesion
Flick middle finger and will see flexion of thumb

163
Q

Management of prolactinomas

A

Dopamine agonists eg. Cabergoline, bromocriptine

164
Q

Management of focal seizures

A

1st line- lamotrigine or levetiracetam

2nd line- carbamazepine, oxcarbazepine or zonisamide

165
Q

Management of tonic clinic seizures

A

Males- Valproate
Females- lamotrigine or levetiracetam

NB- valproate can be considered for girls under 10/those who won’t have children

166
Q

Management of absence seizures

A

first line: ethosuximide

second line:
male: sodium valproate
female: lamotrigine or levetiracetam

NB- carbamazepine may exacerbate absence seizures

167
Q

Management of neuroblastoma

A

Refer very urgently (within 48 hours) to see the paediatrician

168
Q

Complex regional pain syndrome

A

Progressive/disproportionate symptoms to original injury/surgery
Allodynia
Temperature and skin colour changes
Oedema and sweating
Motor dysfunction

Budapest diagnostic criteria

Physiotherapy
Neuropathic analgesia
Pain team input

169
Q

GCS Motor response

A

6- obeys commands
5- localised to pain
4- withdraws from pain
3- abnormal flexion to pain
2- extension to pain
1- none

170
Q

GCS Verbal

A

5- orientated
4- confused
3- words
2- sounds
1- none

171
Q

GCS Eye opening

A

4- spontaneous
3- to speech
2- to pain
1- none

172
Q

Features of hydrocephalus

A

Hydrocephalus presents in infants with an increasing head circumference (splaying of the skull plates allowed by unfused sutures), bulging fontanelles, impaired upward gaze (‘sunsetting’; caused by pressure on the tectal plate), dilated scalp veins, bradycardias, seizures and coma.

173
Q

Management of neuropathic pain

A

First-line treatment for neuropathic pain is amitriptyline (TCA), duloxetine (SSRI), gabapentin (anticonvulsant) or pregabalin (anticonvulsant. If one of these agents don’t work next line is to try one of the other remaining three drugs

NB- trigeminal neuralgia responds best to carbamazepine

NB- also incorporate physiotherapy, CBT, capsaicin cream, tramadol for short term rescue of flare ups

174
Q

Features of a focal seizure

A

Hallucinations
Memory flashbacks
Déjà vu
Doing strange things on autopilot

175
Q

Features of generalised tonic clonic seizures

A

There is loss of consciousness and tonic (muscle tensing) and clonic (muscle jerking) episodes. Typically the tonic phase comes before the clonic phase. There may be associated tongue biting, incontinence, groaning and irregular breathing.

Prolonged post ictal period

176
Q

Types of seizure

A

Generalised- involve neural network on both sides of the brain. Can be motor or non-motor eg. tonic-clonic (grand mal), tonic, clonic, typical absence (petit mal), atonic (someone who drops suddenly, possible incontinent and a post-ictal period that follows). No awareness

Focal- these start in a specific area, on one side of the brain. Can be classified as being motor (e.g. Jacksonian march), non-motor (e.g. déjà vu, jamais vu; ) or having other features such as aura. Awareness can vary

177
Q

Features of a myoclonic seizure

A

Sudden brief muscle contractions, like a sudden “jump”. The patient usually remains awake during the episode

Juvenile myoclonic epilepsy

178
Q

Features of an atonic seizure

A

They are characterised by brief lapses in muscle tone. These don’t usually last more than 3 minute- “drop attacks”

Lennox-Gastaut syndrome

179
Q

Causes of neuropathic pain

A

Postherpetic neuralgia from shingles is in the distribution of a dermatome and usually on the trunk
Nerve damage from surgery
Multiple sclerosis
Diabetic neuralgia typically affects the feet
Trigeminal neuralgia
Complex Regional Pain Syndrome (CRPS)
Lumbar radiculopathy

180
Q

2 drugs that can be used in certain brain tumours

A

Bromocriptine- prolactin-secreting tumours
Ocreotide (somatostatin analogues)- growth hormone-secreting tumours (acromegaly)

NB- surgery is first line in acromegaly, whereas drugs are first line in prolactinomas

181
Q

Anticipation

A

Huntington’s chorea displays something called genetic “anticipation”. Anticipation is a feature of trinucleotide repeat disorders. This is where successive generations have more repeats in the gene, resulting in:

Earlier age of onset
Increased severity of disease

182
Q

Lambert-Eaton myasthenic syndrome

A

Muscle weakness similar to MG, caused by SCLC, muscle weakness improves on repeated action

NB- Voltage-gated calcium-channel antibodies

183
Q

Charcot Marie Tooth disease

A

Inherited condition- presents in childhood (AD)

High foot arches (pes cavus)
Distal muscle wasting causing “inverted champagne bottle legs”
Weakness in the lower legs, particularly loss of ankle dorsiflexion
Weakness in the hands
Reduced tendon reflexes
Reduced muscle tone
Peripheral sensory loss

184
Q

Causes of peripheral neuropathy

A

ABCDE

Alcohol
B12 deficiency
Cancer and Chronic Kidney Disease
Diabetes and Drugs (e.g. isoniazid, amiodarone and cisplatin)
Every vasculitis

185
Q

Features of GBS

A

back/leg pain in the initial stages of the illness
progressive, symmetrical weakness of all the limbs.
-the weakness is classically ascending i.e. the legs are -affected first
-reflexes are reduced or absent
-sensory symptoms tend to be mild (e.g. distal paraesthesia) with very few sensory signs

there may be a history of gastroenteritis
respiratory muscle weakness
cranial nerve involvement
-diplopia
-bilateral facial nerve palsy
-oropharyngeal weakness is common
autonomic involvement
-urinary retention
-diarrhoea

186
Q

Todds paresis

A

Patients with focal seizures may experience post-ictal weakness (Todd’s paresis)

A focal weakness, typically of the frontal lobe (motor strip), may occur following a focal-onset seizure

During a focal seizure, patients can either be aware or unaware of their surroundings.

187
Q

Polyneuropathy vs mononeuritis multiplex

A

Mononeuritis multiplex- pattern of involvement is asymmetric

Polyneuropathy- symmetric

188
Q

Lumbar puncture and raised intracranial pressure

A

If a LP is performed with raised ICP, there is a risk of coning. Thus, you wouldn’t perform one if there was evidence of papilledema or clinical signs and symptoms (pain when coughing, early morning etc.) eg. in suspected meningitis with evidence of papilledema, just start antibiotics

189
Q

Management of Stevens-Johnson syndrome

A

Cease all provoking medications, obtain IV access and begin fluid hydration

190
Q

Hoover’s sign

A

If a patient is genuinely making an effort, the examiner would feel the ‘normal’ limb pushing downwards against their hand as the patient tries to lift the ‘weak’ leg. Noticing this is indicative of an underlying organic cause of the paresis. If the examiner, however, fails to feel the ‘normal’ limb pushing downwards as the patient tries to raise their ‘weak’ leg, then this is suggestive of an underlying functional weakness, also known as ‘conversion disorder’.

191
Q

Cranial nerve control

A

Contralateral

192
Q

6 tests to confirm brain death

A

pupillary reflex, corneal reflex, oculo-vestibular reflex, cough reflex, absent response to supraorbital pressure, and no spontaneous respiratory effort

193
Q

L5 radiculopathy vs CNP lesion

A

in L5 radiculopathy, eversion tends to be spared

194
Q

2 distinct causes of hypopituitsim

A

Sheehan’s syndrome (due to PPH)
Pituitary apoplexy (due to tumour)

195
Q

Criteria for CT following head injury

A

CT head immediately

GCS < 13 on initial assessment
GCS < 15 at 2 hours post-injury
suspected open or depressed skull fracture.
any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
post-traumatic seizure.
focal neurological deficit.
more than 1 episode of vomiting

CT head scan within 8 hours of the head injury - for adults with any of the following risk factors who have experienced some loss of consciousness or amnesia since the injury:

age 65 years or older
any history of bleeding or clotting disorders (or on warfarin)
dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs)
more than 30 minutes’ retrograde amnesia of events immediately before the head injury

NB- A patient with GCS <8 or = to 8 needs urgent neurosurgical review. Especially when an open fracture is present.

NB- suspicion of C spine injury, CT c spine

196
Q

Head injury management

A

Raised ICP and waiting for theatre- IV mannitol
Diffuse cerebral oedema- decompressive craniotomy
No Burr holes
ICP monitoring is mandatory for GCS 3-8 and abnormal scan (recommended even if scan is normal)
Cerebral perfusion in adults- above 70
Cerebral perfusion in children- 40-70

197
Q

Jacksonian march

A

Focal seizures starts in one area eg. fingers, then moves progressively (as the electrical activity moves across the brain)

Can lead to secondary tonic-clonic seizure

198
Q

Focal seizure with impaired awareness vs absence seizures

A

Focal seizure with impaired awareness will have prodrome and post-ictal phase (absence seizures occur and terminate rapidly)

199
Q

Management of a myoclonic seizure

A

males: sodium valproate
females: levetiracetam

myoleve (remember like that)

200
Q

Management of tonic/atonic seizure

A

males: sodium valproate
females: lamotrigine

201
Q

Ulnar paradox

A

The ulnar paradox: proximal lesions of the ulnar nerve produce a less prominent deformity than distal lesions (ie. distal lesion will worsen during recovery, before improving)

202
Q

Coning

A

‘Coning’ refers to an uncal herniation as a result of raised intracranial pressure. In this case, as the subdural haemorrhage pushes the brain through the tentorium, uncal herniation is causing damage to the 3rd cranial nerve. This nerve is vulnerable due to its anatomical position predisposing it to external compression by the tentorium.

3rd nerve palsy/down and out gaze

203
Q

Sciatica

A

No more gabapentin/anticonvulsants/SNRI’s- use NSAIDs and weak opioids (and exercise, surgery etc.)

204
Q

SAH and LP

A

If a CT head scan done within 6 hours of symptom onset and reported and documented by a radiologist shows no evidence of a subarachnoid haemorrhage:

do not routinely offer a lumbar puncture

think about alternative diagnoses and seek advice from a specialist.

1.1.12If a CT head scan done more than 6 hours after symptom onset shows no evidence of a subarachnoid haemorrhage, consider a lumbar puncture.

1.1.13Allow at least 12 hours after symptom onset before doing a lumbar puncture to diagnose a subarachnoid haemorrhage.

205
Q

LP Timings

A

Suspected bacterial meningitis: an LP should be done before IV antibiotics, unless:
cannot be done within 1 hour
signs of severe sepsis or a rapidly evolving rash
significant bleeding risk
signs of raised intracranial pressure

206
Q

Unilateral UMN Pathology

A

Intracranial – stroke, SOL → hemisensory loss
Brainstem – stroke, SOL → may be crossed signs
Spinal cord – MS, infarct/haemorrhage, SOL, disc prolapse, trauma, syringomyelia, congenital → sensory-level/segmental sensory loss

207
Q

Bilateral UMN Pathology

A

MS
Motor neurone disease → normal sensation
Myelopathy – cord compression (e.g. due to cervical myelopathy, SOL, disc prolapse, paraspinal infection), trauma, transverse myelitis, syringomyelia, congenital → sensory-level/segmental sensory loss
Others – brainstem stroke, hereditary spastic paraplegia, cerebral palsy, HTLV-1, syphilis

208
Q

Unilateral LMN Pathology

A

See helpful diagram

209
Q

Bilateral LMN Pathology (with distal weakness)

A

Abnormal sensation distally i.e. sensorimotor polyneuropathy

ABCDE:

Alcohol
B12/thiamine deficiency
Charcot-Marie-Tooth, Carcinomas (paraneoplastic)
Diabetes, Drugs (e.g. TB drugs, metronidazole/nitrofurantoin, vincristine/cisplatin, amiodarone)
Every vasculitis (e.g. SLE, RA, polyarteritis nodosa) and some infections (e.g. herpes zoster, HIV, leprosy, syphilis)

Normal sensation i.e. distal motor neuropathy

Chronic inflammatory demyelinating polyneuropathy
Myotonic dystrophy
Inclusion body myositis (proximal in legs but distal in arms)
Progressive muscular atrophy
Lead poisoning
Porphyria

Acute flaccid paralysis

Guillain-Barré syndrome
Some rare infections (e.g. rabies, polio, West Nile)
Cauda equina syndrome
Spinal cord shock

210
Q

Bilateral Proximal Weakness (normal sensation)

A

DENIM:

Dystrophies – Becker’s/Duchenne, limb girdle, facioscapulohumeral (shoulder, face and truncal weakness)
Endocrinological – Cushing’s syndrome, hyper/hypothyroidism, diabetic amyotrophy (lower limbs)
Neuromuscular – myasthenia gravis (fatigable), Lambert–Eaton myasthenic syndrome
Inflammatory – dermato-/polymyositis, inclusion body myositis (proximal in legs but distal in arms), viral myositis
Metabolic/congenital/mitochondrial myopathies

211
Q

Mononeuritis Multiplex

A

Vasculitis – granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis, polyarteritis nodosa, microscopic polyangiitis
Autoimmune – RA, SLE, cryoglobulinaemia, Sjögren’s syndrome, paraneoplastic
Infectious – Lyme disease, HIV, leprosy
Others – diabetes mellitus, amyloidosis, sarcoidosis

212
Q

UMN and LMN Pathology

A

Motor neurone disease (no sensory deficit)
Dual pathology (e.g. cervical myelopathy + polyneuropathy)
Myeloradiculopathy
Subacute combined degeneration of the cord

213
Q

UMN and LMN Pathology

A

Motor neurone disease (no sensory deficit)
Dual pathology (e.g. cervical myelopathy + polyneuropathy)
Myeloradiculopathy
Subacute combined degeneration of the cord

214
Q

Cerebellar Pathology

A

MAVIS:

MS
Alcohol
Vascular – thromboembolic, haemorrhagic
Inherited – Friedreich’s ataxia, spinocerebellar ataxia, ataxia telangiectasia
SOL

215
Q

Parkinsonism

A

Parkinson’s disease
Vascular parkinsonism
Parkinson-plus syndromes: multi-system atrophy, progressive supranuclear palsy, corticobulbar degeneration, Lewy body dementia
Other causes: antidopaminergic drugs, Wilson’s disease, communicating hydrocephalus, supratentorial tumours

216
Q

Horner’s Syndrome

A

Central lesions

Anhidrosis of the face, arm and trunk

Stroke
Syringomyelia
Sclerosis (Multiple)
SOL
Encephalitis

Pre-ganglionic lesions

Anhidrosis of the face

Tumour (Pancoast)
Thyroidectomy
Trauma
Cervical rib

Post-ganglionic lesions

No anhidrosis

Carotid artery dissection
Carotid aneurysm
Cavernous sinus thrombosis
Cluster headache

NB- STC

217
Q

Third Nerve Palsy

A

Pupil-Sparing;

DM
HTN
Ischaemic

Non-Pupil-Sparing (ie. dilated pupil);

Idiopathic
Tumour
Trauma
Cavernous sinus thrombosis
Posterior communicating aneurysm (pupil dilated, often associated pain)
Raised ICP
MS

218
Q

UMN and LMN Signs

A

see helpful diagrams

219
Q

Subacute Combined Degeneration of Spinal Cord

A

B12 deficiency
Mixed UMN and LMN signs

weakness
joint position and vibration sense lost first then distal paraesthesia
upper motor neuron signs typically develop in the legs, classically extensor plantars, brisk knee reflexes, absent ankle jerks

220
Q

CMT

A

LMN signs

High-arched feet (pes cavus)
Hammer toes
Foot drop
Champagne bottled legs
Distal muscle weakness
Distal muscle atrophy
Hyporeflexia

221
Q

GBS

A

LMN signs
Progressive symmetrical weakness of limbs
reflexes are reduced or absent
sensory symptoms tend to be mild (e.g. distal paraesthesia) with very few sensory signs

222
Q

Cauda equina

A

LMN (not the CNS, its the peripheral nerves (PNS) that come off the spinal cord)
low back pain
bilateral sciatica
reduced sensation/pins-and-needles in the perianal area
decreased anal tone
urinary dysfunction
incontinence is a late sign that may indicate irreversible damage

223
Q

Myelopathy

A

UMN (spinal cord)

224
Q

Radiculopathy

A

LMN ie. sciatica

Year 4 Additional Notes (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions