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Neurology Flashcards

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USMLE® Step 1 flashcards
1
Q

Differential diagnosis of Headaches

A 
Migraine,
Tension headaches,
Cluster headaches,
Temporal Arteritis/ GCA,
Medication Overuse headaches,
Meningitis,
Encephalitis, 
Subarachnoid haemorrhage,
Sinusitis
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2
Q

If the patient presents with ‘Thunderclap headaches’, what is the most worrisome differential diagnosis

A

Subarachnoid haemorrhage

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3
Q

Facial nerve palsy: Defintion

A

Isolated dysfunction of the facial nerve. This typically presents with a unilateral facial weakness

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4
Q

CN7 pathway & branches

A

The facial nerve exits the brainstem at the cerebellopontine angle. On its journey to the face it passes through the temporal bone and parotid gland.

Branches: Temporal, Zygomatic, Buccal, Marginal mandibular, Cervical

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5
Q

CN7 Function

A

There are three functions of the facial nerve: motor, sensory and parasympathetic.

Motor: Supplies the muscles of facial expression, the stapedius in the inner ear and the posterior digastric, stylohyoid and platysma muscles in the neck.

Sensory: carries taste from the anterior 2/3 of the tongue.

Parasympathetic: it provides the parasympathetic supply to the submandibular and sublingual salivary glands and the lacrimal gland (stimulating tear production).

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6
Q

Facial nerve palsy: UMN vs LMN lesion

Why is it important to distinguish between them?

A

UMN: forehead- sparing (each side of forehead is innervated by both sides of then brain)

LMN: non-forehead sparing (each side of forehead only supplied by LMN from one side of brain)

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7
Q

LMN facial palsy: presentation

A

On affected side:
No-movement of forehead
Drooping eyelids, exposing eye
loss of nasolabial folds

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8
Q

UMN facial nerve palsy: causes & 2 main conditions/syndrome

A

UMN lesion: strokes, space-occupying lesion (tumour/ bleed)
Bilateral UMN lesions (rare): MND & pseudobulbar palsies

Conditions:Bell’s palsy & Ramsey Hunt syndrome

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9
Q

Bell’s palsy:cause, diagnosis, prognosis & management

A

Cause: idiopathic

Prognosis: Most recover completely but 20-30% have permanent facial weakness or paralysis

Diagnosis: Unilateral facial weakness with no identifiable cause

Management: 10 day Prednisolone 25mg BD within 72 hrs. Anti-virals (eg. acyclovir/ valacyclovir) not indicated. Lubricating eyedrops to prevent eye from drying out. . If they develop pain in the eye they need an ophthalmology review for exposure keratopathy. Tape can be used to keep the eye closed at night.

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10
Q

Ramsey Hunt syndrome: cause, presentation & management

A

Cause: (cephalic/varicella) Herpes Zoster Virus
Presentation: unilateral facial weakness with painful, tender vascular rash around ear, ear canal and can extend down anterior 2/3 of tongue and hard palate. auditory dysfunction. taste perceptionn and lacrimation may also be affected

Management: Prednisolone & Acyclovir/valacyclovir within 72 hours. Lubricating eyedrops also required

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11
Q

Bilateral LMN facial nerve palsy: common causes

A

Lyme disease & GBS

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12
Q

Most common causes of unilateral vs bilateral facial nerve palsy

A

Unilateral: Herpes zoster (Ramsey-Hunt syndrome)

Bilateral: Lyme disease (bacteria: Borrelia burgdoferi) & GBS

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13
Q

A 40-year-old man comes to the emergency department because of bilateral facial weakness during the past 3 days. He also reports a change in
taste
sensation. One month ago, he had
flu-like
symptoms after returning from a climbing trip in New York. Physical examination shows flattening of the
skin
of his forehead. Motor examination shows difficulty with facial movements bilaterally, including smiling and raising his eyebrows. The remainder of the examination shows no abnormalities. Which of the following is the most likely diagnosis?

A

Major takeaway

Bilateral facial nerve palsy is often associated with untreated Lyme disease. Unilateral palsy is often idiopathic and may be associated with herpes zoster
infection.

Main explanation

This patient’s symptoms of facial weakness, loss of wrinkling of the forehead, and change in taste sensation are consistent with a bilateral facial nerve (cranial nerve VII) palsy. Bilateral facial nerve palsy is rare compared to unilateral involvement and is most commonly associated with Lyme disease and Guillain-Barré syndrome. Patients typically have a sudden onset of symptoms, which can be concerning for a stroke; however, most patients will make a full recovery, with signs of recovery seen within 3 weeks. Lyme disease is a tick-borne illness caused by the bacteria Borrelia burgdorferi. The disease is endemic to the northeastern United States and is often seen in hikers or others who spend time outdoors. Patients may report an initial flu-like syndrome that often goes ignored. The classic sign is erythema migrans, a “bulls-eye”rash with central clearing. If untreated, cardiac and neurologic manifestations, including bilateral facial nerve palsy, may occur.

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14
Q

Causes of LMN CN7 palsy

A

Infection: Otitis media, Malignant otitis externa, HIV, Lyme’s disease

Systemic disease: Diabetes, Sarcoidosis, Leukaemia, Multiple sclerosis, Guillain–Barré syndrome

Tumours: Acoustic neuroma, Parotid tumours, Cholesteatomas

Trauma: Direct nerve trauma, Damage during surgery, Base of skull fractures

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15
Q

Dementia: Definition

A

Acquired, progressive cognitive impairment involving one/more cognitive functions.

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16
Q

Dementia: examples of cognitive and non-cognitive effects

A

Cognitive functions: language, comprehension, judgement and planning & other executive functions

Non-cognitive effects: personality, mood, emotional control, behaviour & psychosis

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17
Q

Dementia: Types of functional impairment

A

Agnosia: ability to recognise objects, persons, sounds, shapes or smells

Anosognosia: lack of ability to perceive the reality of one’s own deterioration

Apraxia: inability to perform learned (familiar) movements on command, even though the command is understand and there is willingness to perform task

Apathy: lack of feeling and interest

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18
Q

Dementia: Risk factors

A

Key: advancing age

Non-modifiable

  • Age
  • Genetics
  • PMHx: Hearing loss & depression

Modifiable

  • Cognitive reserve: leaving education early, less job complexity & social isolation
  • Increased inflammation: central obesity and infection
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19
Q

Dementia: Early stage

A

Often overlooked as gradual onset.

Common symptoms

  • forgetfulness
  • losing track of time
  • becoming loss in familiar places

Can be attributed to normal aging

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20
Q

Dementia: Middle stage

A

Presentation becomes clearing

  • forgetful of recent events and people’s names
  • becoming confused while at home
  • having increased difficulty with communication
  • needing help with personal care
  • experiencing behaviour changes, including wandering and repeated questioning
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21
Q

Dementia: late stage

A

Near total dependence and inactivity. Memory disturbances are serious and physical signs and symptoms becoming more obvious

  • becoming unaware of time and space
  • having difficulty recognising relatives and friends
  • having an increasing need for assisted self-care
  • having difficulty walking
  • experiencing behaviour changes that may escalate and include aggression
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22
Q

Dementia: Types and distribution

A

Alzheimers: 50-70%
Vascular Dementia: 20-30%
DLB: 10-25%
FTD: 10-15%

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23
Q

Dementia: Differential histology findings

A

Alzheimers:

  • extracellular accumulation of senile plaque (amyloid peptides): vessel wall deposits correlate with injury
  • Intraneuronal neurofibrillary tangles (NFTs): Better predictor of cognitive decline
  • Neuronal loss

Vascular dementia:

  • cerebral artery atherosclerosis
  • carted artery/heart embolisation
  • vasculitis
  • small white matter infarcts (Brain MRI) (absent cortical atrophy)

DLB:
- Alpha-syneiclein protein aggregation in neurons (particularly cortex, substantial nigra) -> Lewy bodies -> apoptosis

FTD:
- Associated with specific cellular inclusions: tau proteins (Pick disease) & TDP-43

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24
Q

Dementia: Inx

A

Bloods: FBC, U&E, glucose, LFTs, calcium, ESR & CRP, Folate & B12, TFTs, syphilis serology

Imaging: Chest X-ray, CT/MRI

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25
Q

Dementia: Causes (reversible & non-reversible)

A

Degenerative: Alzheimers, DLB, FTD, Huntington and Parkinson, NPH, Primary progressive aphasia

Vascular: cerebral haemorrhage, cerebral infarct/ atherosclerosis

Metabolic: uraemia, hepatic failure & paraneoplastic syndromes

Endocrine: Hypothyroidism & hypocalcaemia

Toxic: alcohol, o

Infection: syphilis, CJD, HIV, Whipple’s disease

Deficiency: Alcohol excess/withdrawal, folate & B12 deficiency, thiamine

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26
Q

Dementia: Key differential characteristics of Ddx

A

Vascular: ‘step-wise’ decline. CVD risk factors & history

FTD: 40-65 yr old. memory loss develops after behavioural changes/ personality disturbances, language and movement

DLB: Parkinsonism (bradykinesia, tremors and rigidity) developed <1 year after cognitive decline, REM sleep disorder, visual hallucination (early stage)

Alzheimers: advanced age, FHx - gradual memory loss (episodic then romantic)

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27
Q

FTD: 2 most common types

A
  1. Frontal variant: affects behaviour and personality

2. Primary progressive aphasia: language

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28
Q

Alzheimers: Treatment

A
  • Acetylecholinesterase inhibitor: donepezil (mild-moderate), rivastigmine (if main symptom: hallucination)
  • NMDA receptor antagonist (memantine): advanced neuroprotective and DMARD
  • Vitamine E supplements
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29
Q

DLB: Management

A

Goal: Alleviate symptoms

  • Acetylcholinesterase inhibitors: doneprazil & rivastigmine (visual hallucinations)
  • Dopamine analoge (motor symptoms)
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30
Q

FTD: Treatment

A

Goal: Alleviate symptoms

  • Anti-depressants (severe behavioural symptoms)
  • Atypical antipsychotic drugs (significant SE)
  • Atypical antipsychotics eg. haloperidol and risperidone.
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31
Q

Vascular dementia: treatment

A

Vascular risk factor control: anti-HTN, anti-DM, statins, anti-platelet agents

Acetylcholinesterase inhibitors/ memantine

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32
Q

Delirium: Definition & subtypes

A

Clinical syndorme characterised by disturbed consciousness, cognitive function or perception. Acute onset with fluctuation course

Subtypes: Hyperactive (75%), Hypoactive (25%)

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33
Q

Delirium: Causes

A

Surgery

Systemic infection: sepsis, UTI, malaria, pneumonia, IV line/catheter

Intracranial infection/ head injury

Drugs/ drug withdrawal: opiates, levodopa, sedatives, recreational

Alcohol withdrawal (2-5s post-admission; increased LFTs, increased MCV; Hx of EToH abuse

Metabolic: uremia, liver failure, Na+ or glucose, low Hb, malnutrition (beriberi)

Hypoxia: respiratory or cardiac failure

Vascular: stroke, MI

Nutritional: thiamine, nicotinic acid or B12 deficiency

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34
Q

Delirium: DDx

A

Dementia

Psychiatric: schizophrenia, anxiety, epilepsy (non-convulsive status epilepticus = under diagnosed)

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35
Q

Delirium: Inx

A

Goal: Look for cause

Bloods: FBC, ESR/CRP, U&E, Glucose, ABG, septic screen (urine dipstick, CXR, blood cultures)

Consider: ECG, malaria films, Lumbar Punture, EEG & CT

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36
Q

Delirium: Management

A

Identify & treat cause

Other aims:

  • Re-orientate patient; explain where they are and who you are at each encounter
  • encourage family visits
  • monitor fluid balance and encourage oral intake. Beware for constiption
  • Mobilise and encourage physical activity
  • Practice sleep hygiene: restrict daytime napping, minimise might-time disturbance
  • Avoid/ remove catheters, IV cannulae, monitor leads and other devices
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37
Q

Delirium vs Dementia

A

Acute vs Chronic (trends & Hx)

Inattention, Disorganised thinking & Distractibility -> Delirium

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38
Q

Brain metastasis: Prevalence and most common primary sites

A

Affects 40% of patients with cancer

Site: lung, breast, colorectal & melanoma

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39
Q

Brain metastasis: Prognosis

A

Poor prognosis

Median survival: 1-2 months

Better prognosis with single lesion, best cancer

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40
Q

Brain metastasis: Presentation

A 
Space occupying lesion: headache (often worse in morning, when coughing/ bending), 
Focal neurological signs, 
Ataxia,
Fits,
N&V,
Pallioedema
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41
Q

Brain metastasis: Management

A

Imaging: Urgent head MRI/CT

Disease stage and performance status

Reduce cerebral oedema: Dexamethasone 16mg/24hr
Stereotatic radiotherapy

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42
Q

Chronic Fatigue Syndrome: Diagnosis

A

Chronic fatigue ≥ 24 hrs

+ 4 symptoms: myalgia, polyarthralgia, unrefreshing sleep, fatigue after exertion after 24 hrs. decreased memory, persistent sore throat or cervical lymphadenopathy

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43
Q

CFS: Management

A

CBT & graded exercise

Pharmacological management (same as fibromyalgia), shown ineffective for CFS:

  • Amitriptyline - relieve pain and improve sleep
  • Pregabalin - if amitriptyline ineffective
  • Duloxetine or SSRI: co-morbid depression and anxiety

Steriods/ NSAIDs not recommended.. no inflammatory process

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44
Q

CFS: Yellow flags

A

Psychosocial risk factors to developing chronic pain

Belief that exercise will worsen pain
Problems attaining benefits
Social withdrawal
Sickness behaviour eg. extended rest
Overprotective family or lack of support
Emotional problems eg. depression, anxiety / stress
Inappropriate expectations of treatment eg. low active participation in treatment

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45
Q

ME/CFS: Cause

A

Research suspect an infection may trigger ME/CFS: EBV (glandular fever), Ross Rive virus, Coxiella brunetti.
HHV-6, rubella, Candida albicans, bornavirus. mycoplasma and HIV
Bacterial infection: pneumonia

Immune system changes

Hormone imbalanceStress affect body chemistry: HPA axis regulates immune response, digestion, energy usage and mood. Lower cortisol can lead to inflammation and immune suppression (levels normal for CFS patients therefore not diagnostic marker)

Possible genetic link

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46
Q

Encephalitis: Definition

A

Acute inflammation of brain parenchyma due to direct invasion/pathogen-initiated immune response

Often assoc. with meningitis

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47
Q

Encephalitis: Route of infection

A

Peripheral nerve conduits to brain parenchyma for viral infection - rabies, HSV

haematogenous spread -> transfer of infection from distant sites

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48
Q

Encephalitis: Causes

A

Viral: HSV-1 (most common) & HSV-2
EBV, HIV, VZV (varicella-zoster virus), measles, mumps, rabies. influenza

Non-viral: any bacterial meningitis, TB, malaria, syphillis, listeria, Lyme disease, legionella, leptospirosis, aspergillosis

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49
Q

Encephalitis: Risk factors

A

Immunosuppression,
Travel to low-income nations,
Exposure to disease vectors in endemic areas

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50
Q

Encephalitis: Complications

A

Seizures,
SIADH
Increased ICP
Coma

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51
Q

Encephalitis: Presentation

A

General red flags: fever, chills & malaise

Meningeal involvement (meningism): nuchal rigidity, headache & photosensitivity

Parenchymal involvement: focal neurological sings, seizures, altered mental state.

History of travel or animal btes

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52
Q

Encephalitis: Inx

A

Bloods: blood & CSF cultures, glucose, toxoplasma IgM titre, malaria film

Contrast CT: Focal bilateral temporal lobe involvement suggestive of HSV encephalitis. meningeal enhancement suggests meningoencephalitis. Do before LP.
MRI alternative if allergic to contrast

Lumbar puncture: moderately increased CSF protein and lymphocyte and decreased glucose. Send CSF for viral Per including HSV

EEG: urgent EEG showing diffuse abnormalities may help diagnosis of encephalitis but doesn’t indicate cause.

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53
Q

Encephalitis: Treatment

A

Viral encephalitis:

  • HSV: acyclovir
  • CMV: ganciclovir/foscarnet

Bacterial encephalitis
- Targeted antibodies

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54
Q

Encephalitis: Prognosis

A

Mortality in untreated encephalitis is 70%

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55
Q

Cerebral abscess: pathology

A

localised focal necrosis of brain tissue with inflammation, usually caused by bacterial infection

rare (de novo within brain, primary infection typically arises elsewhere, spreads to brain)

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56
Q

Cerebral abscess: Presentation

A

Classic Triad (20% of cases)

  • Fever, progressive worsening focal neurology, headache
  • Increased ICP while supine -> worse headache early morning, at night/ increased ICP stimulates medullary centre, area postrema -> morning vomiting

Mental status change, seizures, nausea & vomiting, papilloedema

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57
Q

Cerebral abscess: Inx

A

CT/MRI (eg. ring-enhancing lesion)

Bloods: Increased CRP, ESR & wCC.

Special: Abscess aspirate - biopsy, LP (increased WCC = increased protein concentration, normal glucose content)

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58
Q

Cerebral abscess: Treatment

A

Urgent neurosurgical referral: Drainage & removal of foreign material

Medication

  • Targeted Abx therapy: penetration through abscess wall poor, typically accompanies surgical management
  • Hyperbaric O2 therapy: reduce ICP, bacteriostatic, enhances oxidative immune function
  • Corticosteroid in complicated cases with pituitary insufficiency
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59
Q

Diabetic Neuropathy: Defintion

A

Peripheral nerve damage secondary to DM.

Depending on affected nerves, diabetic neuropathy symptoms: pain & numbness in legs, feet and hands. It can also cause problems with digestive system, urinary tract, blood vessels and heart.

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60
Q

Diabetic Peripheral neuropathy: Presentation

A

Distribution: Glove & stocking (most common) distribution. May be patchy

Absent ankle jerks

Neuropathic deformity (Charcot foot): pes cavus, clawed toes, loss of transverse arch, rocker-bottom sole
Caused by loss of sensation -> increased mechanical stress on pressure points  and repeated joint injury. Swelling, instability & deformity.

Painful neuropathy: numbness, burning or shooting pain, tingling and/or paraesthesia of the hands and/or feet typically in a stocking and glove distribution, often at night. Over time it can progress to persistent neuropathic pain

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61
Q

Diabetic Automatic Neuropathy: presentation

A

Can affect multiple systems

Postural hypotension

Gastroparesis (delayed gastric emptying). Unexplained diarrhoea

Inadequate bladder emptying,

Sexual disfunction eg. erectile dysfunction

Sweating abnormalities & impaired awareness of hypoglycaemia

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62
Q

Diabetic Foot: Prevention and services

A

Refer early; podiatry, imaging, vascular surgery

Amputations common (135/week): warn patients & educate to monitor their feet weekly for signs of change eg. using mirror to monitor soles

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63
Q

Diabetic foot: Vascular ischemia vs peripheral neuropathy

A

Ischaemia: Critical toes +/- ‘punched out’ ulcers, absent pulses

Neuropathy: Injury/ infection over pressure points eg. metatarsal heads.

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64
Q

Diabetic foot: Ischaemia presentation & Management

A

Absent foot pulses
Critical toes; gangrene

Management

  • education
  • regular chiropody: remove callus, as haemorrhage and tissue necrosis may occur below -> ulceration
  • treat fungal infections:
  • surgery eg. endovascular angioplasty balloon, stents & subintimal recanalisation.
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65
Q

Diabetic neuropathy: Foot ulceration

A

Typically painless, punched our ulcer in area of thick callus +/- superadded infection. Causes cellulitis, abscess +/- osteomyelitis

Asses degree of:

  1. Neuropathy (clinically)
  2. Ischaemia (critical toes, absent foot pulse)
  3. Bony deformity eg. Charcot foot (clinically & x-ray)
  4. Infection (swabs, blood culture, x-ray for osteomyelitis, problem ulcer to reveal depth)

Management: regular chiropody. bed rest & therapeutic shoes

  • Charcot’s joints: bed rest/ crutches/total contact cast until oedema and local warmth reduce and bony repair complete ( ≥8 weeks). Bisphosphonates may help
  • Cellulitis: admit for IV Abx. Common organisms: staphs, streps, anaerobes.
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66
Q

Diabetic neuropathy: Charcot’s foot symptoms

A

Swelling
Warmth
Change in foot colour
Change in foot shape: loss of transverse arch, rocker bottom sole.

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67
Q

Diabetic neuropathy: Absolutely indications for surgery in ulcerated foot

A

Abscess/ deep infections
Spreading anaerobic infection

Ischemic Limb: gangrene/rest pain

Suppurative arthritis

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68
Q

Diabetic neuropathy: Four main types

A

Symmetrical sensory polyneuropathy: glove & stocking distribution.

  • tingling & numbness. pain. worsens at night
  • Rx: paracetamol -> Tricycline (amitriptyline) -> Duloxatine -> gabapentin -> opiate

Autonomic neuropathy

  • Postural hypotension
  • Vagal neuropathy: loss of respiratory sinus arrhythmia
  • Gastroparesis
  • Unexplained diarrhoea
  • Gustatory sweating
  • Sexual dysfunction eg. erectile dysfunction
  • Urine retention
Mononeuritis multiplex (eg. CN3 & CN6)
  - If sudden & severe -> Rx: immunosuppressants eg. Prednisolone, IV Ig, ciclosporin

Amyotrophy

  • Muscle wasting of quadriceps muscle +/- pelvifemoral muscles
  • Imaging: electrophysiology.
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69
Q

Epilepsy: Defintion

A

Recurrent seizures of unknown causes. Spontaneous, intermittent and abnormal brain waves.
Convulsions = motor signs of electrical discharges

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70
Q

Epilepsy: elements (prior and post) of seizures

A

Prodrome: lasting hours/days prior to seizure.
- change in mood or behaviour

Aura: can be focal seizure of temporal lobe
- strange feeling of gut, deja vu, strange smells, flashing lights

Post-ictal

  • headache, confusion, and myalgai
  • Todd’s paralysis: temporary weakness after focal seizure in motor cortex
  • dysphasia following focal seizure of temporal lobe
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71
Q

Epilepsy: Causes of epileptic seizure

A

2/3 cases idiopathic
… increased excitation: long-lasting/ fast activation of NMDA receptors via glutamate
… decreased inhibition: genetic mutations -> dysfunction GABA receptors

Disorders: brain injury, brain abscess, brain tumours, eclampsia, encephalitis, Angelman syndrome

CVD: ischaemia stroke, intracranial bleeding, perinatal hypoxia, ischaemia

Systemic disorder: Uremic encephalopathy, hepatic encephalopathy, eletrolyte imbalance (Na, Mg & Ca), hypoglycaemia, thiamine deficiency, Vitamin B12 deficiency

72
Q

Epilepsy: Causes of provoked seizures

SICKDRIFT3R

A

Substrate: glucose, O2
Isoniazid
Cations: Na, Mg & Ca
Kids: pregnancy, eclampsia
Drugs: aminophylline, bupivacaine, bupropion, butyrophenones.
Recreational: amphetamines, cocaine, methylphenidate, psilocybin, psilocin (present in psychedelic mushrooms)
Rum: alcohol +/- withdrawal
Illness (chronic): Tuberous sclerosis, sarcoidosis, SLE, Ig targeting VGKC
Fever: febrile seizures
Trauma
3 anti: histamine, depressants, convulsants
Rat poison

73
Q

Epilepsy: Inx

A

Bedside:

  • EEG
  • Neuro exam: assess behaviour, motor abilities, mental functions
    • > underlying seizure cause & type
  • Glucose
  • Urine sample

Bloods: FBC (WCC - inflammation/ vasculitis), U&E, LFTs, renal function

Imaging: MRI/CT scans
- detect structural abnormalities

74
Q

Epilepsy: Focal vs Generalised. Subtypes.

A

Focal: initially stems from localised brain region; limited to one hemisphere

  • Focal aware: patient awake & alert. No impaired consciousness
  • Focal impaired awareness: unilaterally affects large area of one hemisphere. Individual loses awareness; responsiveness; does not remember seizure. Most commonly in temporal lobe -> post-ictal features
  • 2dary generalised

Generalised: engages both cerebral hemispheres. No localising features referable to single hemisphere.

  • Absence seizure
  • Febrile seizure
  • Tonic
74
Q

Epilepsy: Focal vs Generalised. Subtypes.

A

Focal: initially stems from localised brain region; limited to one hemisphere

  • Focal aware: patient awake & alert. No impaired consciousness
  • Focal impaired awareness: unilaterally affects large area of one hemisphere. Individual loses awareness; responsiveness; does not remember seizure. Most commonly in temporal lobe -> post-ictal features
  • 2dary generalised

Generalised: engages both cerebral hemispheres. No localising features referable to single hemisphere.

  • Absence seizure
  • Febrile seizure
  • Tonic: rigid stage. falls backwards
  • Clonic: convulsion stage
  • Tonic-Clonic: Post-ictal stage included
  • Myoclonic: sudden, brief, involuntary muscle jerks lasting 1-2s.
  • Infantile spasm
  • Atonic: sudden muscle relaxation; forward falling
75
Q

Epilepsy: Localising features of focal seizures

A

Temporal lobe
- Automatisms: complex motor phenomena with impaired awareness
Primitive oral (lip smacking, chewing, swallowing)
Complex actions
- Dysphasia
- Deja vu/ jamais vu (everything seems strangely unfamiliar)
- Emotional disturbance eg. sudden terror, panic anger or elation and derealisation
- Hallucinations of small, taste or sound
- Delusional behaviour
- Bizarre association

Frontal lobe

  • Motor features: posturing or peddling movements of legs
  • Jacksonian march
  • Motor arrest
  • Subtle behavioural disturbances
  • Dysphasia or speech arrest
  • Post-ictal Todd’s palsy

Parietal lobe

  • Sensory disturbances: tingling, numbness, pain (rare)
  • Motor symptoms: die to spread to pre-central gyrus

Occipital lobe
- Visual phenomena: spots, lines & falshes

76
Q

Epilepsy: Management for each syndrome

A

AEDs: only commended after epilepsy diagnosis of ≥2 seizures. Choice depends on subtype, lifestyle, co-morbidities and patient’s preferences

Treat cause: if reversible, known cause

Focal: 1st line: carbamazepine or lamotrigine. 2nd: levetiracetam, oxcarbazepine or sodium valproate

Absence seizures: 1st line: Sodium valporate or ethosuximide (children). 2nd: lamotrigine

Myoclonic: 1st: sodium valporate. 2nd: levetiracetam or topiramate (increased SE). Avoid carbamazepine and oxcabazepine - may worsen

General tonic-clonic: 1st Sodium valporate or lamotrigine. 2nd: carbamazepine. clobazam, levetiracetam or topiramate

Other interventions: Psychological therapies eg relaxation, CBT.

77
Q

Essential tremor: pathology

A

Most common movement disorder: involuntary, rhythmic, shaking

Usual sites: hands, fingers. Sometimes head, vocal cords

Action tremor (occurs during muscle effort)
  - postural/ intention tremor
78
Q

Essential tremor: causes

A

Mainly idiopathic

Familial: autosomal dominant inheritance pattern

79
Q

Essential tremor: Risk factors

A
  • Meat consumption: heterocyclic amines (eg. germane, harmaline) exposure
  • Associated with dystonia (cervical, spasmodic, cranial dystonia, writer’s cramp), parkinsonism
80
Q

Essential tremor: Presentation

A

Rhythmic, symmetrical tremor
- hands, head, vocal cords, neck, face, leg, tongue, trunk
High frequency tremor (4-12Hz) exacerbated by muscle contraction
Inability to perform precise tasks

Intention tremor
- Intensifies upon touching nose with finger

Postural tremor
- during outstretched arms

Walking difficulties
Decreased tremor with alcohol intake

81
Q

Essential tremor: Diagnosis

A

Physical examination

  • Fine postural, active tremor in hands, head/voice
  • Asymmetric/symmetric: cogwheel rigidity, resting tremor, dystonia (esp. head)

Other diagnostic:

  • postural/ action tremor of hands/head; duration ≥ three years
  • alleviation with alcohol intake
82
Q

Essential tremor: Treatment

A

Medications: If disabling, symptomatic treatment

  • Beta-blockers: propranolol
  • Anti-epileptics: Primidone. 2nd line: Gabapentin and topiramate
  • Benzodiazepine: alprazolam or clonazepam
  • Botulinum toxin (hand tremor not responsiveness to medication)

Lifestyle Modification

  • avoid caffeine, nicotine etc
  • get enough sleep
83
Q

Essential Tremor vs Parkinson’s tremor

A

Laterally: Symmetrical vs Asymmetrical
Kinetics: Movement/posture vs Resting
Speed: High frequency vs Slow
Involvement: Arms, legs, voice, neck, face & tongue vs Hands, legs & chin

84
Q

Meniere’s Disease: pathology

A

Increased pressure in endolymphatic system of inner ear.

Causing vertigo, progressive hearing loss

85
Q

Meniere’s Disease: Causes

A

Exact cause unknown: likely abnormal fluid, ion homeostasis in inner ear (endolymphatic hydrops)

Possibly due to endolymphatic sac/ duct blockage, viral infection, vestibular aqueduct hypoplasia, vascular constriction

86
Q

Meniere’s Disease: Risk factors

A

Children - congenital inner-ear malformation

FHx: 10% familiar

87
Q

Meniere’s Disease: Presentation

A

Recurrent vertigo lasting >20min
Fluctuating (or permanent) sensorineural hearing loss
Tinnitus
(with sense of fullness +/- falling to one side)

Associated symptoms: fatigue, nausea & vomitting

Less common: drop attack

88
Q

Meniere’s Disease: Diagnosis

A

Diagnostic criteria:

  • 2+ unprovoked vertigo episodes (each lasting >20 mins)
  • Audio-metrically confirmed sensorineural hearing loss in affected ear on at least one occasion before/during/after vertigo attack
  • Tinnitus/fullness feeling in ear
89
Q

Meniere’s Disease: Management

A

Pharmacological:

  • Antihistamines - cinnarizine, buccal prochlorperazine if severe
  • Antiemetics,
  • Anticholinergics

Surgery: if symptoms don’t improve
- surgical decompression of endolymphatic sac

Other interventions

  • Sodium restrictoin
  • Diuretics
90
Q

Meningitis: Defintion

A

inflammation of meninges coning CSF. Mainly caused by bacterial/ viral infection

91
Q

Meningitis: Meningococcal septicaemia

A

Meningococcus bacterial infection of bloodstream

Causes ‘non-blanching rash’ (maculopapular): caused by DIC (disseminated intravascular coagulopathy) and subcutaneous hemmorhages

92
Q

Meningitis: Bacterial causes

A

Most common in children & adults

  • Neisseria meningitidis (meningococcus)
    • diplococci
  • Streptococcus pneumonia (pneumococcus)

Neonates: Group B Streptococcus (GBS)
- usually contracted during birth as present in mother’s vaginal canal

93
Q

Meningtis: Presentation

A

Insidious onset with fever, malaise, N&V

Later meningism: headache, vomiting, nuchal/back rigidity, photophobia, altered consciousness

Kernig’s test:
lying the patient on their back, flexing one hip and knee to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees. This creates a slight stretch in the meninges and where there is meningitis will produce spinal pain or resistance to this movement.

Brudzinski’s test:
lying the patient flat on their back and gently using your hands to lift their head and neck off the bed and flex their chin to their chest. A positive test is when this causes the patient to involuntarily flex their hips and knees.

94
Q

Meningitis: Complication

A

Complications up to 20% of patients

  • sensorineural hearing loss
  • imparted vestibular funciton
  • epilepsy
  • diffused brain injury
95
Q

Meningococcaemia: Presentation

A

Mild: Fever, maculopapular rash w/out shock

High-grade: pyrexia and septic shock within 6-12hrs due to rapidly escalating endotoxin levels
  - Circulatory failure
  - coagulopathy with skin haemorrhage
  - thrombosis of extremities/adrenals
  - AKI
  - ARDS
\+/- meningism
96
Q

Meningococcaemia: Complications

A 
Amputation,
Skin necrosis,
Pericarditis, 
Arthritis,
Ocular infection,
Pneumonia (esp. serotype Y & W),
Permanent adrenal insufficiency
97
Q

Meningitis: Management (Inx & Management)

A

Start Abx immediately if suspected.

Intra & extracellular diplococci on microscopy: CSF/blood/skin lesion
PCR: CSF/ blood/ skin lesion

Treatment: urgent Abx treatment

  • If non-blanching rash in 1st care: Benzylpenicillin
  • 1st line: ceftriaxone
  • Other bactericidal: cefotaxime, chloramphenicol, meropenem

Prevention:

  • routine infant vaccination against capsular group C in UK
  • capsular group B vaccination

Prophylaxis of contacts:

  • ciprofloxacin/ ceftriaxone (single dose)
  • rifampicin 600mg BD or 48h
98
Q

Viral meningitis: Causes & presentation compared to bacterial

A

Most common:
- Herpes simplex virus (HSV),
- Enterovirus and varicella zoster virus (VZV).
A sample of the CSF from the lumbar puncture should be sent for viral PCR testing.

Viral meningitis tends to be milder than bacterial and often only requires supportive treatment.

99
Q

Viral meningitis: Treatment

A

Aciclovir can be used to treat suspected or confirmed HSV meningitis

100
Q

Meningitis: Lumbar puncture results (bacterial vs viral)

A

The spinal cord ends at the L1-L2 vertebral level so the needle is usually inserted into the L3-L4 intervertebral space.

Appearance: Cloudy vs Clear
Protein: High vs Mildly raised or normal
Glucose: Low vs normal
White Cell Count:  High (neutrophils) vs High (lymphocytes)
Culture:  Bacteria vs Negative
101
Q

Meningitis: Complications

A

Sensorineural hearing loss,
Cognitive impairment & learning disability
Seizures & Epilepsy
Memory loss
Focal neurological deficit: limb weakness/ spasticity

102
Q

MND: Defnition

A

Progressive, ultimately fatal condition where motor neurones stop function. Characterised by selective loss of neurones in motor cortex, cranial nerve nuclei and anterior horn cells
No effect on sensory neurones and patients should not experience any sensory symptoms.

103
Q

MND: Differentiation from MS, polyneuropathies and myasthenia

A

MS & polyneuropathy:MND has no sensory loss or sphincter disturbance
Myasthenia: MND has no effect on eye movements

104
Q

MND: 4 clinical patterns

A

ALS/ amyotrophic lateral sclerosis (80%)

  • loss of motor neurones in motor cortex and anterior horn of cord
  • combined UMN & LMN signs
  • worse prognosis if: bulbar onset, increased age & decreased FVC

Progressive bulbar palsy (10-12%)
- only affects CN 9-12

Progressive vascular atrophy (<10%)

  • LMN only: anterior horn cell lesion
  • affects distal muscle group before proximal
  • prognosis: better than ALS

Primary lateral sclerosis (rare)

  • Loss of Betz cells in motor cortex: mainly UMN signs
  • marked spastic leg weakness and pseudobulbar palsy
  • no cognitive decline
105
Q

MND: Presentation

A

Think MND in >40 yrs (median UK age 60M) with stumbling spastic gait, foot drop +/- proximal myopathy, weak grip and shoulder abduction or aspiration pneumonia

UMN signs: spasticity, rigidity, brisk reflex and upping plantar response

LMN: muscle wasting, reduced tone, fasciculation (tongue, abdomen, back & thigh) and reduced reflexes

Bulbar signs: dysarthria

106
Q

MND: Diagnosis

A

Based on clinical presentation and exclusion

Brain/ cord MRI to exclude structural cause
LP: exclude inflammatory cause
Neurophysiology: detect subclinical denervation and help exclude mimicking motor neuropathy

107
Q

MND: Prognosis

A

Poor: <3 years post onset for 50% of patients

108
Q

MND: Management

A

No effective treatments for halting/ reversing disease… MDT approach

Riluzole (Inhibit glutamate release and NMDA receptor antagonist)

  • slow progressive of disease
  • extend survival by a few months

Symptomatic treatment:

  • Excess saliva: advice on positioning oral care and suctioning. Try anti-muscarinic (eg. propantheline) or Botulinim may help
  • Dysphagia: blend food, gastrostomy is an option
  • Spasticity: exercise, orthotics
  • Communication difficulty: provide alternative communication method
  • Palliative care
109
Q

Multiple sclerosis Definiton

A

Inflammatory plaques of demyelination in the CNS disseminated in space and time in multiple sites. Neurodegenerative condition involving demyelination of neurones and poor healing leading to axonal loss.

This is caused by an inflammatory process involving the activation of immune cells against the myelin.

110
Q

MS: Classic Demographic

A

Typically presents in:

  • young adults (under 50 years). Median 30hrs
  • more common in women: 3:1

Symptoms tend to improve in pregnancy and in the postpartum period.

111
Q

MS: Neurones affected

A

Schwann cells in:

CNS: oligodendrocytes

112
Q

MS: Causes

A

Causes unknown… hypothesis: vitamin D & role of infection

Genetics: multiple genes
Infection: EBV (epstein barr virus)
Low Vitamin D
Smoking Obesity

113
Q

MS: Common Presentation

A

Usually mono-symptomatic:
- 20% present with unilateral optic neuitis: pain on eye movement and decreased rapid central vision
Common: involvement if corticospinal tract & bladder

Symptoms worsen with heat

114
Q

MS: Other presentation

A

Focal weakness

  • Bells palsy
  • Horners syndrome
  • Limb paralysis
  • Incontinence
  • erectile dysfunciton & anorgasmia

Focal sensory symptoms

  • Trigeminal neuralgia
  • Numbness
  • Paraesthesia (pins and needles)
  • Lhermitte’s sign: electric shock sensation that travels down the spine and into the limbs when flexing the neck. indicates disease in the cervical spinal cord in the dorsal column. It is caused by stretching the demyelinated dorsal column.

Ataxia

  • Sensory ataxia: result of loss of the proprioceptive sense, which is the ability to sense the position of the joint (e.g. is the joint flexed or extended).
    - This results in a positive Romberg’s test and can cause pseudoathetosis.
  • Cerebellar ataxia is the result of problems with the cerebellum coordinating movement. This suggestions cerebellar lesions.
115
Q

MS: Disease patterns

A

Highly variable between individuals

Clinically isolated syndrome: first ep. of demyelnation & neurological presentation. May not develop MS

Relapsing-remitting: most common pattern at initial diagnosis

  • Active: new symptoms/ lesions are appearing on MRI
  • Not active: no new symptoms or MRI lesions are developing
  • Worsening: overall worsening of disability over time
  • Not worsening: there is no worsening of disability over time

Secondary Progressive: RR developing into progressive worsening of symptoms with incomplete remissions.
Symptoms become more permanent.
- Active: new symptoms/ lesions are appearing on MRI
- Not active: no new symptoms/ MRI lesions
- Progressing: overall worsening of disease over time (regardless of relapses)
- Not progressing: there is no worsening of disease over time

Primary Progressive: worsening of disease and neurological symptoms from the point of diagnosis without initial relapses and remissions.
Similar classification as secondary progressive

116
Q

MS: Diagnosis

A

Neurologist based: clinical picture & symptoms suggesting lesions that change location over time
Symptoms progressive over a period of 1 year to diagnose primary progressive MS. Other causes for the symptoms need to be excluded.

Investigations:

  • MRI scans: demonstrate typical lesions
  • Lumbar puncture can detect “oligoclonal bands” in CSF
117
Q

Optic Neuritis: Presentation

A

Unilateral reduced vision developing over hours to days
Key features are:
- Central scotoma. This is an enlarged blind spot.
- Pain on eye movement
- Impaired colour vision
- Relative afferent pupillary defect

118
Q

Optic neuritis: defintion

A

Inflammation of the optic nerve

119
Q

Optic Neuritis: Causes

A 
Multiple sclerosis is the main cause,
Sarcoidosis,
Systemic lupus erythematosus (SLE)
Diabetes,
Syphilis,
Measles,
Mumps,
Lyme disease
120
Q

Optic Neuritis: management

A

Urgent referral to ophthalmologist after acute vision loss

Treatment: Steroids (Prednisone) 2-6 weeks

121
Q

Optic neuritis: Complciation

A

50% of patient develop MS over next 15 years.

MRI changes can predict likelihoo

122
Q

MS: Management

A

MDT: neurologist, specialist nurse, physiotherapist, occupational health other others

Education: Condition and treatment

Disease-modifying drugs:
- Mild RR MS: Dimethyl fumarate, Alemtuzumab (Monoclonal Antib. acts against T cells) and natalizumab (acts against VLA-4 receptors that allow immune cells to cross BBB),
Azathioprine is not recommended due to its SE profile.
- Treating relapses: Methylprednisolone, eg 0.5–1g/24h IV/PO for 3–5d shortens acute relapses; use sparingly

Symptom control:
- Spasticity: baclofen or gabapentin.
2nd line: Tizanidine or dantrolene
if these fail consider benzodiazepines.
- Tremor: botulinum toxin type A injections
- Urgency/frequency: if post-micturition residual urine >100mL, teach intermittent self-catheterization; if <100mL, try tolterodine.
- Fatigue: amantadine, CBT, and exercise may help.

123
Q

MG: Defintion

A

Myasthenia graves is an autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest.

124
Q

MG: Antibody involved

A

85%: Ab against nicotinic acetylcholine receptors (AChR)
Location: post-synaptic NMJ
15%: Ab against muscle-specific kinase (MuSK) & low-density lipoprotein receptor related protein 4 (LRP4).
- fewer proteins to make AChR receptor
Both B&T cells indicated

125
Q

MG: Presentation

A

Muscle weakness worsen with exertion and improves with rest. Symptoms minimal in morning and worse at end of day.

Mostly affect proximal muscles and small muscles of the head and neck:

  • Extraocular muscle: diplopia
  • Eyelid weakness: ptosis
  • Weakness in facial movements
  • Difficulty with swallowing
  • Fatigue in the jaw when chewing
  • Slurred speech
  • Progressive weakness with repetitive movements
126
Q

MG: Exacerbating factors

A 
Pregnancy, 
hypokalaemia,
infection,
change of climate,
emotion,
exercise,
Drugs: gentamicin, opiates, tetracycline, quinine & beta-blockers, over treatment
127
Q

MG: Associations

A

Autoimmune diseases (RA and SLE)

if <50 yrs: more in women & thyme hyperplasia
> 50 yrs: more in men & thyme atrophy tunic tumour

128
Q

MG: Examination (elicit fatigue)

A
  • Repeated blinking will exacerbate ptosis
    • Prolonged upward gazing will exacerbate diplopia on further eye movement testing
    • Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides

Check for a thymectomy scar.

Test the forced vital capacity (FVC).

129
Q

MG: diagnosis

A

Ab testing:

  • ACh-R antibodies (85% of patients)
  • MuSK antibodies (10% of patients)
  • LRP4 antibodies (less than 5%)

Imaging: CT/ MRI of thymus gland for thymoma.

Edrophonium test: helpful where doubt is present.

130
Q

MG: Treatment

A
  • Reversible acetylcholinesterase inhibitors (usually pyridostigmine or neostigmine)
    • Immunosuppression (e.g. prednisolone or azathioprine)

Surgery: Thymectomy can improve symptoms even in patients without a thymoma

Monoclonal antibodies

  • Rituximab: Monoclonal antibody targeting B cells and reduces the production of antibodies.
  • Eculizumab is a monoclonal antibody that targets complement protein C5. This could potentially prevent the complement activation and destruction of acetylcholine receptors. (not NICE recommended)
131
Q

MG: Myasthenic crisis

A

Severe complication & can be life threatening.

It causes an acute worsening of symptoms, often triggered by another illness such as a RTI leading to respiratory failure as a result of weakness in the muscle of respiration.

132
Q

Myasthenic crisis: Management

A

Ventilation: non-invasive ventilation with BiPAP or full intubation and ventilation.

Medical treatment: immunomodulatory therapies (IV Ig) and plasma exchange

133
Q

Parkinson’s: Pathology

A

Degeneration of dopaminergic neurones in substantial nigra -> dopamine depletion from basal ganglia

Protein (alpha-synuclein) accumulation in neuron. Build up of Lewy bodies in neurones accompanied by death of astrocytes

134
Q

Parkinson’s: Extrapyramidal triad

A
  1. Tremor: resting tremor; pin-rolling
  2. Hypertonia: rigidity + tremor = ‘cogwheel’ rigidity
  3. Bradykinesia: slow to initiate movement
135
Q

Parkinson’s: Causes

A

Usually idiopathic,
Genetic loci: PINK1 mutation, Parkin, alpha synuclein gene,
Toxicity in recreational drugs MPPP (rare)

136
Q

Parkinson’s: Risk factors

A

Mean onset: 80-85 yrs
PMHx: previous head injury, pesticide exposure.
FHx

Protective factors: nicotine & caffeine

137
Q

Parkinson’s: Presentation

A

Triad: tremor, bradykinesia, Hypertonia

Non-motor symptoms:
Autonomic dysfunction (postural hypotension, constipation, urinary frequency/urgency, dribbling of saliva),
Sleep disturbance,
Reduced sense of smell (common 1st symptom)

Neuropsychiatric: common & debilitating
Depression
Dementia
Psychosis

138
Q

Parkinson’s: Diagnosis

A

Clinical diagnosis
- Triad presentation & dopaminergic medication response
- Exclude: cerebellar disease & FTD/ DLB
Postmortem autopsy

Imaging: MRI to exclude other structural defects

139
Q

Parkinson’s: Treatment

SALAD

A

Symptom management

Selegiline
Anticholinergics: (improves neurochem. imbalance)
- trihexyphenidyl, benzhexol, orphenadrine
L-Dopa + peripheral decarboxylase inhibitor:
- carbidopa, benserazide
Amantidine (anti-viral - known NMDA agonist)
Dopamine postsynaptic receptor agonist:
- bromocriptine, lisuride, pergolide

Surgery: Deep brain stimulation (DBS)

  • Increase motor output of basal ganglia -> decrease motor symptoms
  • Severe disease

Other intervention

  • Education, support
  • Physical therapy
140
Q

Parkinson’s: Complication

A

Freezing phenomenon: progressive hypokinesiai & bradykinesia -> akinetic pauses In movement

Falls: 2nd to postural instability, poor movement amplitude

Dystonia: abnormal tone across joint

Dementia: common after prolonged, primarily motor disease
( > 1 yr post memory deficit onset)

141
Q

Peripheral Neuropathy: Specific causes (DAVID)

A 
Diabetes Mellitus (most common)
Alcoholism
Vitamin B12 deficiency 
Infection: GBS, EBV, leprosy, sarcoidosis
Drugs eg. isoniazid, amiodarone, pyridoxine, nitrofurantoin
142
Q

Peripheral Neuropathy: 6 main mechanism

A
  1. Demyelination – e.g. GBS, post-diphtheric neuropathy, hereditary sensory-motor neuropathies
    – usually occurs as a result of schwann cell damage.
  2. Axonal degeneration
    – usually occurs in toxic neuropathies
    – conduction speed remains normal, and the axon tends to dies of peripherally first, then more proximally. Surviving axons often strive to re-innervate affected areas
  3. Wallerian degeneration: fibre degeneration when the fibre is cut or crushed.
    - Both the axon & myelin sheath will degenerate over several weeks after the incident.
  4. Compression: e.g. carpal tunnel syndrome
    – there is local demyelination at the site of compression. Occurs when the compression is not as severe as in wallerian degeneration.
  5. Infarction: polyarteritis nodosa, Churg-Strauss syndrome, diabetes
    – there will also be wallerian degeneration distal to the infarct.
  6. Infiltration – e.g. leprosy, malignancy, inflammation, sarcoidosis
143
Q

Peripheral neuropathy: presentation

A

Altered sensation, pain, weakness or autonomic symptoms
Symptoms normally start distally -> Proximal

Classic picture of advanced polyneuropathy:

  • distal wasting & weakness
  • absent tendon reflexes
  • glove & stocking sensory loss
143
Q

Peripheral neuropathy: presentation

A

Altered sensation, pain, weakness or autonomic symptoms
Symptoms normally start distally -> Proximal

Classic picture of advanced polyneuropathy:

  • distal wasting & weakness
  • absent tendon reflexes
  • glove & stocking sensory loss
144
Q

Peripheral neuropathy: Distribution

A

Symmetrical, generalised, multifocal or focal

Symmetrical generalised polyneuropathy: distal-to-proximal gradient in “stocking-glove” pattern

Mononeuropathy Multiplex: almost simultaneously dysfunction of several peripheral nerves. Frequently painful and cause weakness.

Focal neuropathy (mononeuropathy): Trauma & entrapment of peripheral nerves.

145
Q

Peripheral neuropathy: Most freq. seen entrapment neuropathies (mononeuropathy)

A

• Median nerve across the wrist (carpal tunnel syndrome)
• Ulnar nerve across the elbow (tardy ulnar palsy)
• Radial nerve at the spiral groove (Saturday night palsy)
• Peroneal nerve at the fibular head (peroneal nerve palsy)
• Distal branches of the tibial nerve at the ankle (tarsal tunnel
syndrome)

146
Q

Peripheral Neuropathy: Inx

A

Bloods:

  • Urine: glucose & protein. Heavy metal screen (Hg, Pb, Zn & As)
  • Haematology: FBC, ESR, vitamin B12 & folate
  • Biochemistry: Fasting BGC, Renal function, LFT, TSH

Neurophysiological tests: Assessment of distal & proximal nerve stimulation
Biochemistry: Serum protein electrophoresis, serum ACE
Immunology: Anti-nuclear factor, Anti-extractable nuclear antigen antibodies (anti-Ro, anti-La), anti-neutrophil cytoplasmic antigen ab)

Imaging: CXR - screen for asymptomatic LC

147
Q

Sensory Neuropathy: Cause and presentation

A

Cause: DM, CKD, leprosy

Presentation: numbness, paraesthesia, difficulty handing small objects

  • Glove & stocking distribution
  • Signs of trauma or joint deformation may indicate sensory loss

Diabetic & Alcoholic neuropathies can be painful

148
Q

Motor Neuropathy: Cause and Presentation

A

Case: GBS, lead poisoning. Charcot-Marie-Tooth syndrome

Presentation:

  • Often progressive (may be rapid)
  • Weak/ clumsy hand
  • Difficulty in walking (falls/ stumbling)
  • Difficulty breathing (decreased FVC)

Signs
- LMN: muscle wasting and weakness in distal muscles of hands & feet (foot/ wrist drop). Reflexes reduced/ absent

149
Q

Peripheral neuropathy: Pharmalogical Treatment

A

Treating Cause

  • GBS & CIDP: IV Ig & corticoid steroids (pred. for CIPD only)
  • Vasculitis: steroids/ immunosuppressants (Azathioprine, methotrexate, cyclophosphamide)
Neuropathic pain (Tricyclic): amitriptyline, duloxetine, gabapentin or pregabalin
  - Use: bring, dysesthetic pains with peripheral neuro.

Anticonvulsants: carbamazepine, phenytoin & lamotrigine.
- Treat lancinating pain with trigeminal neuralgia

150
Q

Peripheral Neuropathy: Support Intervention

A

Involve physiotherapy and occupational therapy

Foot care and shoe choice - aim to reduce trauma

151
Q

Radiculopathy: Definition

A

Conduction block in axons of spinal nerve or its roots, with impact on motor axons causing weakness and on sensory axons causing paraesthesia &/or anaesthesia

NOT SPINAL CORD (cord compression) therefore more localised effect

152
Q

Radiculopathy: Causes of nerve compression

A

Intervertebral disc prolaspe: rupture of annulus fibrosis and sequestration of disc material

Degenerative diseases of spine: lead to neuroforaminal or spinal canal stenosis

  • Cervical spine = most mobile segment of the spine and degenerative change is a normal part of ageing process
  • 80% of the population over 55 years old have degenerative changes between C5/6 and C6/7

Fracture: trauma/ pathological

Malignancy: most commonly metastatic (lung, breast, prostate and kidney)

Infection: extradural abscess, osteomyelitis (Pott’s disease) or herpes zoster

153
Q

Radiculopathy: Presentation

A

Sensory features: paraesthesia and numbness
Motor features: weakness
Radicular pain often present
- Typically described as a burning, deep, strap-like, or narrow pain. It is not uncommon for radicular pain to be intermittent.

Identify red flags: faecal incontinence, urinary retention, saddle anaesthesia

154
Q

Radiculopathy: Presentation vs Location of impingement

A

C5 (C4/5 disc)

  • Motor/ sensory: weak deltoid & supraspinus. Decreased supinator jerks; numb elbow
  • Pain: neck/ shoulder that radiates down from front of arm to elbow

C6 (C5/6 disc)

  • M/S: weak biceps & branchioradialis; decreased bicep jerks, numb thumb & index finger
  • Pain: shoulder radiating down arm below elbow

C7 (C6/7 disc)

  • M/S: weak triceps & finger extension; decreased tricep jerks; numb middle finger
  • Pain: upper arm and dorsal forearm

C8 (C7/T1)

  • M/S: weak finger flexors & small muscle of hand; numb 5th & ring
  • Pain: upper arm and medial forearm
155
Q

Radiculopathy: Definitive LT Mangement

A

Definitive long-term management depends on the underlying cause. Only condition requiring emergency surgical is CES.

Most IV disc prolapses managed non-operatively

Indications for surgical treatment

  • Unremitting pain despite good conservative management
  • Progressive weakness
  • New/progressive myelopathy (Spinal cord compression)
156
Q

Radiolopathy: Symptomatic Mangement

A

Analgesia using WHO analgesic ladder in the first instance.

However neuropathic pain meds. are frequently used.

  • 1st line: Amitriptyline. Alternative: pregabalin & gabapentin
    - SE: Muscle spasms managed with diazapam / baclofen.

Physiotherapy remains an important part of management in this patient group.

157
Q

Spinal Cord compression: Definition

A

Malignant cord compression: radiological evidence of indentation of the thecal sac secondary to cancer.

158
Q

Anatomy: Vertebral level of end of spinal cord

A

L1/L2

159
Q

Spinal cord compression: Cancers associated with SCC 2nd to metastatic disease

A

Lung, Breast, kidney, prostate and thyroid cancer

160
Q

Spinal cord compression: Causes

A

Malignant compression (Primary and Secondary)

Other causes:

  • Trauma
  • Intervertebral disc prolaspe
  • Haematoma
  • Epidural abscess (2ndary to osteomyelitis/ discitis)
  • Cervical spondylitis myelopathy
161
Q

Spinal Cord Compression: Presentation

A

Requires high degree of suspicion: presentation can be subtle
- pain, motor and sensory symptoms & bladder and bowel involvement

Cord compression: Back pain, paralysis, hyperreflexia, positive babinski’s

Cauda equina: Back pain, radiculopathy, reduced anal tone, saddle anaesthesia, paralysis, hyporeflexia, hypotonia.

162
Q

Spinal Cord Compression: Diagnosis

A

Imaging: MRI for suspected malignant cord compression

  • determination of extent of disease
  • accurate identification of site of compression

Other possible modalities:

  • Myelography
  • Computed tomography
  • Bone scan
  • Plain radiographs

Bloods: FBC & coagulation screen, inflammation markers, B12, syphillisserp;pgu, u&E, LFT, PSa, serum electrophoresis

163
Q

Spinal Cord Compression: Management

A

Acute cord compression & CES = surgical emergencies

General measures:

  • Analgesia
  • Refractory pain: Refer to pain team
  • VTE prophylaxis
  • TED stockings na prophylactic LMWH

Urgent Dexamethasone - malignancy (& receive oedema)
- Radio/chemo therapy dependant on tumour type +/- decompressive laminectomy

Epidural abscess -> surgically decompressed and Abx

164
Q

Stroke: Prevalence

A

Common medical emergency.

  • Total strokes: ~ 110,000/ yr
  • 11% mortality rate after 1st stroke
  • 1/2 survivors suffer with permanent disability
Ischaemic stroke (85%): occlusion of vessels
Haemorrhage (15%): bleeding
165
Q

Stroke: Definition

A

Cinical syndrome characterised by sudden onset of rapidly developing focal or global neurological disturbance
- Lasting > 24 hours/ death.

166
Q

Stroke: Causes

A

Ischaemia

  • Thrombosis: local blockage by atherosclerosis
    - Precipitating: CVD risks or small vessel disease (vasculitis, sickle cell)
  • Emboli: AF or carotid artery disease, endocarditis, dialted cardiomyopathies, rheumatic valve disease
  • Dissection (rare): spontaneous/ 2dary to trauma

Haemorrhage:

  • HTN (most common)
  • Non-traumatic ICH: vascular malformation (AV malformation/ fistula), brain tumour, vasculitis/ bleeding disorders. Aneurysm rupture, anti-coagulant/ thrombolysis
  • Trauma
167
Q

Haemorrhagic stroke: Presentation

A

Global features:

  • Headache
  • Altered mental state
  • Nausea & Vomiting
  • Hypertension
  • Seizures

Focal neurological deficits (dependent on location of bleed)

168
Q

Cerebral Ischaemic stroke: Location & Differential presentation

A

Anterior:

  • Unilateral weakness and/or sensory deficit: face (leg>arm)
  • Homonymous hemianopia
  • Higher cerebral dysfunction: dysphasia, visuospatial dysfunction (e.g. neglect, agnosia). impaired judgement and incontinency

Middle:

  • Unilateral contralateral weakness: face & (arms>leg)
  • Slurred speech (dysphagia)
  • hemispatial neglect
  • homonymous hemianopsia
  • deviation of eye to left side

Posterior: vertebrobasilar arterial system

  • Dizziness
  • Diplopia
  • Dysarthria & Dysphagia
  • Ataxia
  • Visual Field defects
  • Brainstem syndromes: often seen with crossed signs*
169
Q

Posterior stroke syndromes: 2 main types

A

Brainstem syndrome:

Wallenberg syndorme: Posterior inferior cerebellar artery syndrome (PICA)

  • dizziness, nystagmus, speech, swallowing difficulties
  • Ipsilateral: facial sensory loss, Horner’s sign & ataxia
  • Contralateral: loss of pain, temperature sensation in limbs

Locked in syndrome: Basilar artery

  • dizziness, gait, vision disorders, dysarthria, dysphagia
  • plegia of head, body muscles, except eye; only blinking and vertical movement possible
170
Q

Wallenberg syndrome/ Lateral medullary syndorme: Features

A
  • Nystagmus
  • Vertigo
  • Ipsilateral Horner’s syndrome
  • Ipsilateral facial sensory loss
  • Dysarthria & dysphagia
  • Diplopia
  • Contralateral pain and temperature loss
171
Q

Lacunar infarcts: Locations and 5 syndromes associated

A

Location: Basal ganglia, internal capsule, thalamus & pons

5 syndrome: ataxic hemiparesis, pure motor, pure sensory, sensorimotor and dysartheria/ clumsy hand
Cognition/ consciousness intact except thalamus infant

172
Q

Stroke: Diagnosis

A

Urgent referral: stroke unit

Imaging Head CT/MRI:

  • Urgent < 1hr: if haemorrhagic stroke suspected
  • Less urgent < 24hrs

NIHSS score & clinical history

Bedside: observations, blood glucose, ECG (AF)
Bloods: FBC, U&Es, Bone profile, LFT, ESR, coagulation, lipid profile, HbA1c
Imaging: CT head +/- CT angiography +/- MRI head
Special: Echocardiography, carotid dopplers, 24 hour tape, young stroke screen

173
Q

Stroke: DDx (stroke mimics)

A

Toxic/metabolic: hypoglycaemia, drug & alcohol consumption

Neurological: seizure, migraine, Bell’s palsy

Space occupying lesion: tumour, haematoma

Infection: meningitis/encephalitis, systemic infection with ‘decompensation’ of old stroke

Syncope: extremely uncommon presentation of TIA, many other causes

Non-organic: functional neurological disorders (FND)

174
Q

Stroke: NIHSS score

A

Out of 42: predictive score of clinical outcome in stroke
- Imp. in considering thrombolysis in clinical outcome

Score <4: good clinical outcome
Score >22 (high): significant proportion affected by ischaemia
- higher risk of haemorrhage with thrombolysis (contra.)

175
Q

Stroke: Management

A

Establish blood flow in ischaemic penumbra

  • Thrombolytic enzymes: rtPA, alteplase given wtihin 4.5 hrs
  • Antiplatelet: aspirin +/- clopidogrel

Hypertension treatment
-IV Labetalol/ nicardipine

cerebral oedema managment

  • Antipyretic: if temperature > 39C
  • IV insulin: hyperglycaemia

Medical Conditions (8 decks)

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