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Phase 3a Tera Pyo Edition > Neuro (3A) > Flashcards

Neuro (3A) Flashcards

1
Q

What is presbycusis

A

Age related sensorineural hearing loss

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2
Q

What is otosclerosis

A

Autosomal dominant replacement of normal bone with spongy vascular bone.

  • Conductive deafness
  • Tinnitus
  • “Flamingo tinge” to tympanic membrane
  • Family history
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3
Q

What is meniere’s disease

A

Recurrent episodes of vertigo, tinnitus and sensorineural hearing loss, lasting mins-hours. Vertigo main complaint!

  • Middle aged adults
  • Feeling of aural fullness/pressure
  • Nystagmus/positive romberg test
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4
Q

Investigations in Meniere’s disease

A

Menieres triad
- Otoscopy - Normal ear drum
- Audiometry - Sensorineural hearing loss
- Tympanometry - normal

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5
Q

Pharmacological management of Meniere’s

A
  • Betahistine medication (H1 agonist that acts as a Vestibular sedative)
  • Prochlorperazine (acute vertigo and nausea)
  • Intratympanic gentamicin injection if surgical
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6
Q

What is acoustic neuroma

A

AKA vestibular schwanomma. Tumour arising from schwann cells myelinating CN8. Usually presents between 40-60yo.

Associated with type 2 neurofibromatosis

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7
Q

How can acoustic neuroma present

A

Depends on cranial nerves affected
- CN5: Absent corneal relfex
- CN7: Facial palsy
- CN8: Unilateral sensorineural hearing loss and tinnitus, vertigo.

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8
Q

Investigation of acoustic neuroma

A

Audiogram and examination show sensorineural hearing loss.

MRI Gold standard imaging for diagnosis and tumour tracking.

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9
Q

Management and complications of acoustic neuroma

A
  • Conservative or
  • Tumour excision or
  • Radiotherapy
  • Permanent hearing loss (CN8), permanent facial weakness (CN7)
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10
Q

What is an essential tremor, give features and management

A

Autosomal dominant condition usually affecting both arms.

  • Postural tremor: worse when arms stretched out
  • Improved by alcohol and rest
  • Most common cause of titubation (head tremor)

Managed with propanolol, or primidone second line

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11
Q

How does left heart failure cause right heart failure

A

Left side of heart is unable to pump efficiently, causing blood to back up into pulmonary veins and arteries. This increases pulmonary blood pressure. This pressure is then transmitted back towards the right ventricle.

The dilation of the right ventricle stretches the AV valve, causing a regurgitation into the right atrium during systole. This causes right atrium dilation, which puts further pressure on the right ventricle causing it’s hypertrophy. Eventually neither work efficiently causing right heart failure. RHF causes an increase in blood backing up into general circulation

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12
Q

How does right heart failure cause its cardinal symptoms

A

Jugular vein distension - Increased pressure in right atrium is transmitted back to the jugular veins

Hepatomegaly - Increased pressure of the hepatic veins, which usually directly drain into the inferior vena cava

Peripheral pitting oedema - Increased pressure in the systemic venous circulation, forcing fluid out of the blood into surrounding tissues

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13
Q

Signs and symptoms of left heart failure

A

Signs
- Tachypnoea, tachycardia
- Cool peripheries
- Peripheral cyanosis
- Pink frothy sputum/crackles on auscultation
- Wheeze
- Third heart sound
- Displaced apex beat

Symptoms:
- Dyspnoea, Orthopnoea (SOB when lying flat), Paroxysmal nocturnal dyspnoea (SOB at night)
- Fatigue and weakness
- Weight loss

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14
Q

Signs and symptoms of right heart failure

A

(usually due to pathology involving lungs/pulmonary vessels e.g. pulmonary stenosis)

Signs (due to backing up of fluid):
- Raised JVP
- Peripheral pitting oedema (thighs, sacrum, abdomen)
- Hepatosplenomegaly
- Ascites
- Facial engorgement
- Pulsing in face/neck (tricuspid regurgitation)

Symptoms:
- Fatigue/weakness
- Swelling in legs/distended abdomen
- Nausea/anxiety
- Nose bleed

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15
Q

How does left heart failure cause pulmonary oedema, and how does this lead to right sided heart failure

A

LV unable to move blood out into body, causing backlog.
This increases blood stuck in LA, pulmonary veins and lungs. They leak fluid as a result and are unable to reabsorb it. This causes pulmonary oedema; lung tissues and alveoli become full of interstitial fluid, interfering with gas exchange, leading to SOB and other symptoms.

Pulmonary HTN puts pressure on right ventricle, meaning it isn’t able to pump as much blood, causing right sided heart failure.

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16
Q

How might a heart failure patient present on examination?

A
  • Increased resp rate
  • Reduced O2 saturation
  • Tachycardia
  • Hypotension
  • Dyspnoea
  • Oedema in legs

Auscultation:
- 3rd heart sound/ displaced apex beat
- Bilateral basal crackles (that sound wet)

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17
Q

Investigations in Heart failure

A

BNP (Brain Natriuretic Peptide) blood test
- Released from stressed ventricles in response to increased mechanical stress
- (NOT specific, also released in tachycardia, sepsis, PE, renal impairment, COPD)

CXR (ABCDE)
- Alveolar Oedmea, Kerley B lines (interstitial oedema), Cardiomegaly, Dilated upper lobe vessels, Pleural effusion

ECG will show wide QRS and may help diagnose causation

Echocardiography is KEY. Measures Ejection fraction, ventricular function, valvular abnormalities

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18
Q

Scoring system for heart failure functional limitations

A

New York Heart Association classifications of heart failure

I (Mild) - No limitation on physical activity. Ordinary physical activity doesnt cause fatigue/palpitations/dyspnoea
II (Mild) - Slight limitation n physical activity. Comfortable at rest; dyspnoea on ordinary activity
III (Moderate) - Less than ordinary activity causes dyspnoea, which is limiting. Rest is fine.
IIII (Severe) - Symptoms present at rest, all activity causes discomfort

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19
Q

3 cardinal non specific signs in heart failure

A

SOB AS FAT
Dyspnoea, Ankle Swelling, Fatigue

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20
Q

Pathophysiology of ischaemic, HTN, LV hypertrophy and dilated cardiomyopathy heart failure, and what HF do these cause?

A

Cause systolic failure
- Ischaemic: Myocytes start to die, reducing ability of contraction
- HTN: Arterial pressure increase in systemic circulation means it is harder for LV to pump blood into hypertensive circulation
- LV hypertrophy: increased muscle mass requires increased oxygen supply, more likely muscles will die
- Dilated cardiomyopathy: Heart chambers dilate, become thinner, weaker contractions.

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21
Q

Acute heart failure management

A

Pour SOD

Pour away fluids (Stop fluids)
Sit up
Oxygen
Diuretics
GTN may be needed

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22
Q

Management of chronic heart failure

A

1) ACEi + beta blocker
2) Add spironolactone and SGLT2i if Ejection fraction not controlled with ACEi and BB

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23
Q

What should be kept in mind when prescribing for heart failure? (reg ACEi)

A

ACEi contraindicated in Heart valve disease
ARB (candesartan) can be used instead of ACEi

Aldosterone antagonists added if ejection fraction not controlled with ACEi and BB

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24
Q

How does anterior, middle and posterior cerebral artery stroke present

A

Contralateral weakness/paralysis, sensory loss

Anterior - lower extremities>upper

Middle - Upper>lower, contralateral homonymous hemianopia, aphasia

Posterior - Contralateral homonymous hemianopia with macular sparing and visual agnosia.

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25
Q

Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome)

A

Ipsilateral: facial pain and temperature loss

Contralateral: limb/torso pain and temperature loss

Ataxia, nystagmus

Horner’s also:
- Anhidrosis
- Meiosis
- Ptosis

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26
Q

Anterior inferior cerebellar artery (lateral pontine syndrome)

A

Same as PICA but with added Ipsilateral: facial paralysis and deafness

(PICA:
Ipsilateral: facial pain and temperature loss

Contralateral: limb/torso pain and temperature loss

Ataxia, nystagmus)

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27
Q

What causes locked in syndrome

A

Basilar artery blockage

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28
Q

What does retinal/ophthalmic artery ischaemia cause

A

Amaurosis fugax

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29
Q

What is a lacunar stroke

A

Present with either isolated hemiparesis, hemisensory loss, or hemiparesis with limb ataxia

Strong association with hypertension

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30
Q

What assessment system is used in acute strokes

A

ROSIER (Recognition of Stroke In Emergency Room)

Uses symptoms as + points and mimics (syncope, seizure activity) as - points

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31
Q

Management of ischaemic stroke

A

Once haemorrhagic ruled out:
- IV Alteplase if presents within 4.5 hours
- Mechanical thrombectomy if after 4.5 hours

Then: 300mg Oral aspirin daily for 2 weeks then clopidogrel lifelong daily

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32
Q

What are the driving rules in ischaemic stroke

A

Patients must not drive car for 1 month after TIA or stroke, or 1 year for HGV

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33
Q

Scoring system for risk of stroke after Atrial Fibrillation

A

CHA2DS2 VASc

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34
Q

Define TIA

A

Transient Ischaemic Attack. Acute neurological dysfunction that has a sudden onset and resolves in less than 24 hours.

NOT a stroke as involves ischaemia not infarction

  • Contralateral numbness, face droop, dysphasia, vision loss (Amaurosis Fugax)
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35
Q

What acronym helps identify stroke in public

A

FAST
Face
Arms
Speech
Time

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36
Q

Define amaurosis fugax with pathophysiology and causes

A

Short lived blindness in one eye described as “curtain coming down over vision”. Due to temporary reduction in internal carotid or central retinal artery leading to ischaemia of the retina.

Occurs in GCA, Stroke, AF

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37
Q

What risk score should be completed after TIA

A

ABCD2 - risk of stroke after TIA
Age >60
BP >140/90
Clinical features (unilateral weakness =2, just speech disturbance =1)
Duration >60mins =2, 10-59mins =1

> 6 predicts stroke, immediate referral
4 requires referral

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38
Q

Management of TIA

A

<24 hours since presentation, use DAPT
- 300mg Aspirin and 300mg clopidogrel loading dose
- Followed by aspirin and clopidogrel 75mg for 21 days,
- Then clopidogrel 75mg long term.

May need PPI

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39
Q

What are the types of haemorrhagic stroke

A

Extradural haemorrhage - bleeding above dura mater

Sudural haemorrhage - bleeding between dura and arachnoid

Subarachnoid haemorrhage - bleeding between arachnoid and pia mater

Intracerebral haemorrhage - Bleeding within cerebrum

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40
Q

Important examples of TIA mimics that MUST be excluded

A

Hypoglycaemia - sweating, palpitations, hunger, anxiety. Often has insulin, metformin, sulfonylurea! use. Resolves with insulin

Intracranial haemorrhage - Stroke init. Longer, symptoms get worse instead of better.

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41
Q

General symptoms of haemorrhagic stroke

A

Reduced GCS
Headache
Vomiting
Seizures
One sided arm/leg/face weakness/paralysis

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42
Q

Give the scoring system for unconsciousness

A

Glasgow Coma Scale - assessment of eye opening, verbal and motor response.

Eye out of 4
Verbal out of 5
Motor out of 6

Minimum score 1 per category

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43
Q

Glasgow coma scale scoring system in detail (not sure if need to know but probably helpful to have decent idea)

A

Eye opening
4 - Spontaneous
3 - To speech
2 - To pain
1 - None

Verbal response
5 - Orientated
4 - Confused conversation
3 - Inappropriate words
2 - Incomprehensible sounds
1 - None

Motor response
6 - Obeys command
5 - Localises to pain
4 - Withdraws to pain
3 - Abnormal flexion to pain
2 - Extension of upper and lower limbs to pain
1 - No response

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44
Q

Define Extradural haemorrhage with its main cause and epidemiology

A

Cranial bleeding above the dura mater.

Usually caused by trauma to pterion of skull, causing rupture of middle meningeal artery in temporo-parietal region. Can associate with temporal bone fracture.

Usually found in young adults

Blood doesnt cross suture lines

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45
Q

Why can extradural stroke present slowly at first before becoming more severe

A

If bleeding is slow, symptom onset is slower (lucid interval) before there is a sudden, rapid decline when intracranial pressure increases enough to compress brain

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46
Q

Describe Non contrast CT appearance in Extradural haemorrhage (3)

A
  • Biconvex, hyperdense haematoma
  • Blood doesnt cross suture lines
  • Shows midline shift (increased pressure can cause cause brain shifting/herniation)
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47
Q

What are the main 2 herniation complications of haemorrhagic stroke

A

Supratentorial herniation (cerebrum against skull, compressing arteries and causing ischaemic stroke)

Infratentorial herniation (Cerebellum pushed against brainstem, compressing area that controls consciousness, respiration, heart rate)

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48
Q

What is Cushing’s triad and how is it treated

A

Body’s response to increased intracranial pressure, signifies severe lack of oxygen in brain tissue
- Bradycardia
- Irregular respirations
- Widened pulse pressures (increased systolic, decreased diastolic)

Treated with IV mannitol to reduce ICP

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49
Q

Define Subdural haemorrhage with main cause and epidemiology

A

Bleeding below dura mater, caused by bridging vein rupture.

Usually occur in elderly/alcoholic patients but can occur in babies (shaken baby syndrome)

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50
Q

Causes of bridging vein rupture

A
  • Brain atrophy; with age. Stretches bridging veins, meaning they stretch over gaps unsupported.
  • Alcohol abuse: Causes walls of vein to thin
  • Trauma
  • Falls
  • Shaken baby syndrome
  • Acceleration/deceleration injury
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51
Q

Non contrast CT appearance of Subdural haemorrhage

A

Bleeding between the dura mater and arachnoid
- Follows contours of brain and crosses suture lines, forming a crescent shape

Acute (hyperdense mass)
Chronic (Hypodense mass)
Acute on Chronic (both)

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52
Q

What GCS score requires intubation

A

8 or below

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53
Q

Specific surgical management used in subdural haemorrhage

A

Burrhole washout if haemorrhage small

Craniotomy if large haemorrhage

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54
Q

Define subarachnoid haemorrhage with main cause

A

Bleeding below the arachnoid layer, where CSF is located.

Main cause is a ruptured saccular (or Berry) aneurysm, with majority located between anterior communicating artery and anterior cerebral artery

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55
Q

Risk factors for subarachnoid haemorrhage (7)

A

PKD (Associated with berry aneurysm)
Connective tissue disorders (Ehlers-Danlos, Marfans)
Family history
Increasing age
HTN
Smoking
Alcohol

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56
Q

Typical presentation of subarachnoid haemorrhage

A

Sudden onset occipital “thunderclap” headache, following strenuous activity, with associated neck stiffness and photophobia. Smaller, “Sentinel” headache may have preceded thunderclap

Black, female, 45-70

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57
Q

Signs/symptoms of subarachnoid haemorrhage

A
  • Thunderclap headache
  • Meningism (Headache, photophobia + neck stiffness)
  • Fixed dilated pupil (third nerve palsy - especially in posterior communicating artery rupture)
  • 6th nerve palsy
  • Kernigs and Brudzinskis due to meningism also
  • Nausea/vomiting, weakness, confusion, coma, reduced consciousness, speech reduction
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58
Q

Investigations in subarachnoid haemorrhage

A

Urgent non contrast CT head (blood in subarachnoid space/basal cisterns)
CT angiography to locate bleed source
ECG to detect arrhythmia/abnormality

If CT non conclusive,
- Lumbar puncture (RBCs in CSF and Xanthochromia) 12 hours after onset.

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59
Q

Define Kernigs and Brudzinskis signs

A

Kernig - Inability to straighten bent leg without pain when hip flexed to 90 degrees

Brudzinski - Passive flexion of neck in supine patient elicits hip and knee flexion

Suggest meningitis/meningism

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60
Q

CT Appearance in subarachnoid haemorrhage

A

Blood in subarachnoid space (hyperdense)
- Star shaped lesion (Blood filling in gyro pattern)

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61
Q

Management of Subarachnoid haemorrhage

A

Surgical 1st/GOLD
- Endovascular coiling (clipping also possible but more complications)

Nimodipine to prevent vasopasms
IV Mannitol to reduce ICP
Sodium valproate for seizures

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62
Q

Define meningitis

A

Inflammation of the meninges (specifically leptomeninges - pia and arachnoid). Can be due to viral, bacterial or fungal cause.

Notifiable disease

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63
Q

Viral causes of meningitis

A

More common but less severe
- Coxsackie virus
- HSV (Herpes simplex virus)
- Varicella Zoster virus
- Mumps

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64
Q

Bacterial causes of meningitis

A

Most common - S. pneumoniae and N. meningitidis

Children - ^ and H influenzae

Elderly and pregnant - Listeria Monocytogenes (pregnant avoid cheese)

Newborns - ^ and Group B strep

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65
Q

How do N meningitidis, S pneumoniae, Group B strep and Listeria monocytogenes present on gram film

A

N meningitidis - Gram negative diplococci (Only one that causes non blanching rash!)
S pneumoniae/Group B strep - Gram positive cocci in chains
Listeria monocytogenes - Gram positive bacillus

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66
Q

Signs/symptoms of meningitis

A

Signs
- Neck stiffness, headache, photophobia (avoids light)
- Phonophobia (avoid sound)
- Papilloedema (optic disk swelling)
- Kernig sign
- Brudzinski sign
- Non blanching rash (N meningitidis only)

Pyrexia, reduced GCS

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67
Q

Investigations in meningitis

A

Blood culture 1st line - Bacterial or negative for viral

Lumbar puncture GOLD

Bacterial
- Cloudy/yellow
- Protein high
- Glucose low (<50% normal)
- WCC high (Neutrophil)

Viral
- Clear appearance
- Protein small raise/normal
- Glucose normal (>60% normal)
- WCC high (lymphocytes)

(Gram stain identifies bacteria and CSF PCR identifies viruses)

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68
Q

Fungal appearance of CSF in meningitis

A

Cloudy and fibrous
Protein high
Glucose low
WCC high - Lymphocytes!

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69
Q

Management of bacterial meningitis

A

Primary care: Immediate IV or IM benzylpenicillin (if suspected meningococcal) and hospital referral

Hospital
- Dexamethasone (steroid)
- Cefotaxime or Ceftriaxone IV

  • Give Amoxicillin if under 3 months or over 50 to cover listeria
  • Contact tracing and single dose oral ciprofloxacin for contacts
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70
Q

Complications of meningitis

A

Hearing loss
Seizures
Cognitive impairment
Hydrocephalus
Sepsis

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71
Q

Upper motor neurone lesion signs vs lower motor neurone lesion signs

Type of paralysis
-reflexia
Fasciculations
Babinski sign
Voluntary movement
Muscle tone and power

A

UMN
Spastic paralysis
Hyperreflexia
No fasciculations
Babinski positive
Voluntary movement slowed
Muscle tone and power kept

LMN
Flaccid paralysis
Hyporeflexia
Fasciculations
Babinski negative
Voluntary movement gone
Muscle tone and power lost

(babinski - toes curl up when bottom of foot is stroked
fasiculations - brief spontaneous contractions under skin)

72
Q

Define Multiple sclerosis

A

Type 4 hypersensitivity reaction in which there is autoimmune attack against oligodendrocytes (which create myelin) in the CNS (Brain/Spinal cord). Causes plaques of demyelination.

Lesions vary, meaning plaques are “disseminated in space and time” - affect different areas of CNS at different times/ events.

73
Q

Disease progression types in MS

A
  • Relapsing remitting (most common) - Episodic flare ups without full recovery in between, meaning flares worsen over time. (Most common and often progress to secondary progressive)
  • Secondary progressive - Symptoms start getting worse without remission
  • Primary progressive - Symptoms worsen without remission (/)
  • Progressive relapsing - Constant attack with superimposed flare ups
74
Q

What is Uhtoff’s phenomenon and why does it occur in MS

A

Symptoms worsen with heat (e.g. hot bath) or exercise.

New myelin is inefficient, and doesn’t tolerate temperature rise effectively.

75
Q

What triad is associated with MS

A

Charcot’s neurological triad
- Nystagmus (involuntary side-to-side/up-down rapid eye movements)
- Dysarthria (slowed, slurred speech)
- Intention tremor

76
Q

Signs and symptoms of MS

A
  • Optic neuritis usually first (Loss of vision, eye pain, pale optic disk, double vision)
  • Internuclear ophthalmoplegia (eye muscle paralysis which impairs lateral gaze)
  • Lhermitte’s sign - Electric shock sensation when flexing neck
  • UPPER motor neurone signs
  • Bowel, bladder, erectile dysfunction
  • Ataxia
  • Sensation loss

(Uhthoff’s and Charcot’s neurological triad already mentioned)

77
Q

What criteria is used in diagnosis of MS

A

McDonald criteria (think McDonald’s M!)
- 2 or more relapses with evidence of 2 or more lesions, or one lesion with reasonable history of relapse

78
Q

Investigations in MS (3)

A

MRI Brain/Spine
- Demyelinating plaques (new enhance with contrast, old don’t - showing dissemination in space and time)

Lumbar puncture
- Oligoclonal IgG bands in CSF

Visual evoked potential studies (responses to visual stimulus)
- Shows delayed nerve conduction

79
Q

Management of MS

A

During acute relapse
- Oral/IV methylprednisolone first, cladribine
- Plasma exchange

Maintenance
- Interferon beta
- IV monoclonal antibodies

Cladribine second line in ongoing secondary progressive but causes cancer and is teratogenic

80
Q

Management of complications of MS (3)

A
  • Spasticity - Baclofen and gabapentin
  • Neuropathic pain/depression - amitriptyline
  • Physiotherapy for Spasticity and mobility impairment
81
Q

What are some disease modifying drugs in MS with their indications

A
  • relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaided
  • secondary progressive disease + 2 relapses in past 2 years + able to walk 10m (aided or unaided)
  • IV Natalizumab - monoclonal antibody
  • IV Ocrelizumab
  • Oral fingolimod
  • SC beta interferon
  • SC Glatiramer acetate
82
Q

What is Huntingtons

A

Autosomal dominant trinucleotide repeat disorder, which causes deterioration of nervous system and an excess of dopamine.

Also known as Huntington’s chorea (Chorea= involuntary jerky movements)

HTT gene on chromosome 4 - Mutated Huntingtin proteins aggregate in neuronal cells of caudate and putamen. Causes cell death of GABAergic and cholinergic neruones, causing ACh and GABA deficiency, so less dopamine inhibition. Excess dopamine causes excess movement.

Genetic anticipation - The more copies of the protein DNA polymerase adds on in the sperm, the earlier onset and more severe the disease

83
Q

Signs/symptoms of Huntington’s

A

Usually asymptomatic until 30-50 years
Prodromal - Irritability, depression, cognitive problems
Chorea - Jerky involuntary movements
Eye movement disorders
Dysphagia/dysarthria

Dementia, seizures, death within 15 years

84
Q

Investigations in Huntington’s

A

Clinical diagnosis
- Genetic testing GOLD

                                                                                                                                                                                                                                                        CT/MRI - Caudate and striatal atrophy - increased size of lateral ventricles
85
Q

Other causes of chorea

A

Hyperthyroid
Wilson’s
SLE
Dementia

86
Q

Management of Huntington’s

A

Uncurable

Chorea
- Diazepam and tetrabenazine (Benzodiazepine and dopamine depleting agent)

87
Q

Define Parkinson’s disease

A

Neurodegenerative movement disorder characterised by loss of dopaminergic neurones in Substantia Nigra Pars Compacta of basal ganglia.

Misfolded a synuclein proteins called Lewy bodies also present histologically (dark eosinophilic inclusions)

Causes a dopamine deficiency

88
Q

What are the “parkinsonism” symptoms

A

Resting Tremor
Bradykinesia
Rigidity
Postural instability

89
Q

Signs and symptoms of Parkinson’s (other than parkinsonism)

A

Resting tremor
Cogwheel rigidity
Shuffling gait
Reduced arm swing

Non motor:
Loss of smell
Sleep disturbance
Depression, anxiety
Dementia

90
Q

Investigations in Parkinsons

A

Clinical diagnosis - bradykinesia and 1 other Parkinsonism sign
(Bradykinesia = slow, difficult movements. Smaller handwriting, shuffling gait, reduced arm swing etc)

Dopamine agent trial shows improvement

91
Q

Management of Parkinson’s

A

If Severe: Levodopa + Decarboxylase inhibitor (boost dopamine and Di prevents L-dopa breakdown)
- Co-careldopa (Levodopa and carbidopa)

Otherwise:
Dopamine agonist
- Ropinirole

Monoamine oxidase B inhibitor (MAOBi) (stop breakdown of circulating dopamine)
- Selegiline

92
Q

Complications of Parkinson’s

A

Disease progression and motor fluctuations (off periods when treatment stops working)
- Freezing (sudden stop of movement)
- Dyskinesia
- Dementia

93
Q

Differentials of Parkinsonism

A

Benign Essential Tremor
Wilson’s disease
Encephalitis causing degeneration of substantia nigra
Trauma

94
Q

Define Myasthenia Gravis

A

Type 2 hypersensitivity reaction causing autoimmune destruction of the post synaptic membrane at the neuromuscular junction of skeletal muscle. Antibodies to acetylcholine receptors in 85% of cases. (Anti-AChR)

2x in women.

Mostly affects facial muscles.

Strong association with thymoma/ thymic hyperplasia

95
Q

Signs/symptoms of Myasthenia Gravis (6)

A

Mostly affects proximal and small muscles of head and neck
- Muscle weakness with fatigability, worse with exertion better with rest (e.g. patient counting to 50 will struggle in later numbers)
- Ptosis (eyelid droop) and diplopia (double vision)
- Jaw weakness and weak swallow (dysphagia)
- Head drop
- Facial paresis and slurred speech
- Snarl when attempting to smile (myasthenic snarl)

96
Q

How to check for muscle fatigability on examination (3) and what should you check?

A

Repeated blinking causing ptosis
Counting to 50, speech becomes slurred and quieter towards end
Repeated abduction of one arm will result in weakness in said arm compared to other

Forced Vital Capacity should also be checked

97
Q

Investigations in Myasthenia gravis

A

Antibodies
- AchR antibodies (anti-MuSK and anti-LRP4 less sensitive)
- Anti-MUSK
- Anti LRP4

CT thorax - look for thymus growth/thymoma (rule out)

Tensilon test - Used to be done but causes arrhythmia so dont even think about it

98
Q

What are some drugs that exacerbate MG muscle fatigability

A

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

Most common factor is exertion!

99
Q

Management of Myasthenia Gravis

A

Long acting acetylcholinesterase inhibitor
- Pyridostigmine first line

Immunosuppression (not started at diagnosis, usually started later)
- Prednisolone

Thymectomy may be needed (as many patients also have thymic hyperplasia)

100
Q

Define Guillain Barre Syndrome, with causes

A

Acute autoimmune demyelination of the peripheral nervous system, following an upper resp tract or GI infection (e.g. gastroenteritis)

Acute, symmetrical, ascending weakness!

Can be caused by:
Bacteria:
- Campylobacter Jejuni
- M. pneumoniae

Viral:
- Cytomegalovirus
- EBV

101
Q

Guillain barre disease course (4)

A

Initial GI or URT infection
Symptoms start after 2 weeks
Symptoms peak 2-4 weeks further
Recovery period of months to years

102
Q

Pathophysiology of Guillain Barre syndrome

A

Molecular mimicry.

Pathogenic antigens resemble Schwan cell proteins so when immune response is launched, there is also destruction of myelin sheath. Demyelination occurs in patches down length of axon (segmental demyelination). Schwann cells can remyelinate so patients recover over time. Affects sensory and motor nerves.

103
Q

Signs and symptoms of Guillain Barre syndrome

A

Symptom onset 2-3 weeks after preceding infection. Proximal muscles affected first

Symmetrical ascending weakness beginning in legs/feet.

Areflexia
Reduced sensation
Paraesthesia
Sensory loss
Respiratory distress if lungs affected
Autonomic dysfunction (bowel/bladder, sweating, raised BP/pulse, arrhythmia)

104
Q

Investigations in Guillain Barre syndrome

A

Brighton criteria used to make clinical diagnosis, can be supported by:
- Nerve conduction studies (reduced conduction)
- Lumbar puncture (high protein in CSF, normal cell count and glucose)

Antibodies: subtype of GBS
AIDP (90%) - Anti ganglioside
Miller fisher syndrome (eyes affected first) - anti GQ1b

Do spirometry to assess risk of resp failure

105
Q

Management of Guillain barre syndrome (2 treatments + 2 complication treatments)

A

IV immunoglobulin 5 days (CI if IgA deficiency)
Plasma exchange

VTE Prophylaxis (LMWH)
Ventilation if low FVC

106
Q

Upper motor neurone lesion area

A

Anywhere from pre central gyrus to anterior spinal cord

107
Q

Lower motor neurone lesion area

A

Anywhere from Anterior spinal cord to innervated muscle

108
Q

How is muscle power affected in upper motor neurone lesions?

A

In arms flexors>extensors
In legs extensors>flexors

109
Q

How is organisation of movement conducted

A

1 - Idea of movement in pre motor cortex
2 - Activation of UMN in motor cortex
3 - Impulse via corticospinal tract
4 - Modulation.
- Cerebellum fine tunes and Basal Ganglia green lights signal
5 - Movement and somatosensory info obtained by sensory tracts

110
Q

Types of motor neurone disease

A

Amyotrophic lateral sclerosis (50% of patients)
typically LMN signs in arms and UMN signs in legs
in familial cases the gene responsible lies on chromosome 21 and codes for superoxide dismutase

Primary lateral sclerosis
UMN signs only

Progressive muscular atrophy
LMN signs only
affects distal muscles before proximal
carries best prognosis

Progressive bulbar palsy
palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
carries worst prognosis

111
Q

Presentation of MND

A

asymmetric limb weakness is the most common presentation of ALS
the mixture of lower motor neuron and upper motor neuron signs
wasting of the small hand muscles/tibialis anterior is common
fasciculations
the absence of sensory signs/symptoms
vague sensory symptoms may occur early in the disease (e.g. limb pain) but ‘never’ sensory

112
Q

MG brief pathophys

A

Unexplained destruction of Only UMNs and LMNs.
- No effect on sensory neurones (distinguishing point from MS etc)
- No effect on eyes (distinguishing from myasthenia gravis)
- No cerebellar involvement
- SOD1 mutation association in ALS

113
Q

Management of MND (2) What is prognosis

A

Riluzole (protects neurones from glutamate induced damage)
Respiratory support (non invasive at home)

50% die in 3 years

114
Q

Genetic associations with Alzheimer’s

A
  • APoE e4 - APoE usually helps break down beta amyloid but e4 version less effective.
  • Down’s (Trisomy 21) - Increased APP (amyloid precursor protein) production (APP gene also on C21). APP broken down incorrectly becomes beta amyloid.
  • PSEN1, PSEN2
115
Q

Key histological findings in Alzheimers

A

Senile plaques of beta amyloid proteins (APP incorrectly broken down into sticky, insoluble b amyloid) (extracellular)

Neurofibrillary tangles of hyperphosphorylated tau proteins (intracellular)

116
Q

Signs and symptoms of Alzheimer’s (4)

A

Insidious onset and slow progressive decline

  • Poor memory (short term early, long term late)
  • Speech problems (receptive and expressive dysphagia)
  • Loss of executive function (planning/problem solving)
  • Disorientation/lack of recognition of places, people or objects
117
Q

How would Alzheimers affect behaviour (4)

A

Emotional instability
Depression/anxiety
Withdrawal/apathy
Disinhibition (Socially/sexually inappropriate behaviour)

118
Q

How would Alzheimer’s affect daily living (3)

A

Loss of independence
Early on loss of higher level function (finances, difficulties working)
Later loss of basic function (washing, eating, walking)

119
Q

How is Alzheimer’s diagnosed?

A

Based on DSM-V criteria and MMSE (Mini mental state examination) (25+ normal, <17 severely impaired)

MRI - Generalised brain atrophy with medial temporal then later parietal predominance

Brain biopsy is GOLD but can only be done after death

120
Q

Management of Alzheimer’s

A

Supportive: Improve cognitive function
- Exercise
- Music
- Board games
- Cognitive stimulation program

ACh-esterase inhibitor (Donepezil)
NMDA receptor antagonist (Memantine)

121
Q

Define Vascular dementia

A

Dementia caused by cerebrovascular damage causing hypoperfusion of neuronal cells.

Presents in patients with Stroke/TIA history, UMN signs and general condition decline.

Shows a stepwise decline with symptoms worsening after each cerebrovascular event.

122
Q

Investigations and treatment of vascular dementia

A

Mini mental state exam

CT/MRI of brain
- Multiple cortical and subcortical infarcts
- Atrophy of brain cortex

Treated with management of risk factors (lower BP, cholesterol, diabetes etc)

123
Q

Define Lewy Body Dementia

A

Dementia with Parkinsonism (Resting tremor, bradykinesia, rigidity, postural instability).

Alpha synuclein misfolds in neurones and aggregates to form Lewy Bodies, which deposit in cortex and substantia nigra causing neuron death.

124
Q

Symptoms of Lewy Body Dementia

A

Presents with dementia symptoms first
(memory, focus, speech, understanding issues)

Parkinsonism develops later

Sleep disorders like sleep walking/talking, and hallucinations are also very common in LBD

If Parkinsons first, it is Parkinson Dementia

125
Q

Management of Lewy Body Dementia

A

Dopamine analogue - Levodopa
ACh-esterase inhibitor - Donepezil

126
Q

Define Frontotemporal dementia

A

Focal degeneration of frontal and temporal lobes. Pick’s disease is most common type. Loss of over 70% of spindle neurones.

  • Frontotemporal dementia (Pick’s disease)
  • Progressive non fluent aphasia (Chronic progressive aphasia)
  • Semantic dementia
127
Q

Common features of frontotemporal lobar dementias

A
  • Onset before 65
  • Insidious onset
  • Relatively preserved memory and visuospatial skills
128
Q

What is Pick’s disease, how does it present and what macroscopic and microscopic changes are found

A

AKA Frontotemporal dementia.

Personality change and impaired social conduct! Hyperorality, disinhibition, increased appetite, perserveration beahviours.

Focal gyral atrophy with knife-blade appearance

Macro
- Atrophy of frontal and temporal lobes

Micro
- Pick bodies - spherical aggregations of tau protein (silver staining)
- Gliosis
- Senile plaques and neurofibrillary tangles

129
Q

What is CPA (chronic progressive apahasia)

A

Clues in the name.

Short utterances that are agrammatic. Comprehension preserved

130
Q

What is semantic dementia

A

Fluent progressive aphasia. Speech fluent but empty, not much meaning. Memory better for recent rather than remote events

131
Q

What are pick bodies

A

3R isoform of tau proteins

These become hyperphosphorylated and form tangles, causing atrophy in frontoteporal lobes

(In alzheimers, the isoform is 3R+4R)

132
Q

Give Primary and secondary causes of headache

A

Primary
- Migraine
- Tension
- Cluster

Secondary (to other pathology)
- GCA
- Cerebrovascular disease
- Subarachnoid haemorrhage
- Truma

133
Q

Define Migraine

A

Episodes of recurrent, unilateral throbbing headache. May or may not have an aura and often has visual changes (e.g. photophobia, diplopia etc).

Can last up to 72 hours, and classically preceded by an aura
- Visual, progressive, lasting 5-60 minutes.

134
Q

Common migraine triggers

A

CHOCOLATE
Chocolate
Hangover
Orgasms
Cheese
Oral contraceptive
Lie ins (tiredness)
Alcohol
Tumult (loud noise)
Exercise

135
Q

Signs/symptoms of typical/atypical aura

A

Typical: Lasts 5-60 mins and fully reversible.
- Visual changes (zigzag lines, distortion etc)
- Smell changes
- Paraesthesia

Atypical: >60 mins
- Diplopia
- Motor weakness (hemiplegic migraine!)
- Poor balance
- Reduced consciousness

136
Q

Investigations in migraine

A

Clinical diagnosis:

Migraine with/without aura
(at least 2/4 symptoms, 1 associated symptom, no attribution to another disorder)

CT/MRI to exclude secondary haemorrhage
ESR exclude GCA

137
Q

Treatments of migraine

A

Acute prevention
- Oral Sumatriptan (5-HT receptor agonist (mimic serotonin))
with/without aspirin

Prophylaxis
- Propanolol
- Amitriptyline
- Topirimate (antiemetic)

AVOID Opiates

138
Q

Define Tension headache

A

Most common type of headache.
Bilateral “pressing/tight” headache. Lasts minutes to hours. No associated symptoms except photo OR phonophobia

139
Q

Define cluster headache

A

Severe, unilateral periorbital headache, with associated autonomic features, affecting same side face/eyes. Lasts 15-180 mins.

AKA Trigeminal Autonomic Cephalalgia

140
Q

Signs/symptoms of cluster headache

A

Severe unilateral, periorbital, crescendo headache, lasting 15mins to 3 hours. Clusters of headaches,
(Boring/hot poker pain “worst pain ever”)

Ipsilateral autonomic symptoms
- Ptosis (eyelid droop)
- Miosis (excessive constriction of pupil of eye)
- Teary, bloodshot eye
- Nasal congestion/rhinorrhoea

141
Q

Diagnosis and management of cluster headache

A

Clinical diagnosis (5+ similar headaches)

Acute
- Triptans
- High flow oxygen
(AVOID paracetamol, NSAID, Opioids)

Prophylaxis
- Verapamil (CCB)
- Prednisolone, 2-3 weeks

142
Q

Define trigeminal neuralgia

A

Severe, unilateral “electric” pain along distribution of trigeminal nerve lines. Extremely increased risk in demyelinating disease. Attacks last seconds.

143
Q

Pathophysiology of trigeminal neuralgia

A

Vascular loop (MC superior cerebellar artery) compresses nerve near nerve root entry zone. Compression causes poor conduction along nerve root, causing pain.

144
Q

Common triggers of trigeminal neuralgia pain

A

Light touch (washing, shaving, brushing teeth)
- Talking
- Cold weather
- Spicy food
- Caffeine and citrus

145
Q

What are the branches of the trigeminal nerve

A

Ophthalmic
Maxillary
Mandibular

146
Q

Signs/symptoms of trigeminal neuralgia

A

Facial pain
- Electric/stabbing pain
- Very severe
- Trigeminal distribution
- Unilateral
- Provoked (touch, cold etc)

147
Q

Investigations and management of trigeminal neuralgia

A

Clinical but can MRI brain (space occupying lesion, demyelination etc)

Carbamazepine first line
Surgery (microvascular decompression)

148
Q

Define Cauda Equina

A

Compression of the bundle of nerves below the end of the spinal cord (known as cauda equina). Causes bilateral lower limb weakness/saddle anaesthesia

Medical emergency that requires immediate decompression

149
Q

Signs/symptoms of Cauda Equina

A

Severe lower back pain, bilateral lower limb weakness and reduced sensation. LMN signs!

Saddle anaesthesia (numbness/reduced tone in perianal region, groin, inner thigh)
Decreased reflexes and leg weakness/paralysis
Erectile dysfunction
Bladder/bowel dysfunction.

150
Q

Investigations and treatment of cauda equina

A

URGENT MRI spine GOLD

Emergency decompressive laminectomy (vertebra removal) within 24-48 hours, or permanent weakness/dysfunction

151
Q

Brief overview of the anatomy of the spine

A

Originates at base of medulla oblongata, exiting through foramen magnum, ending at conus medullaris at L2

Consists of 5 sections of vertebrae, with 31 spinal nerves arising from this
- Cervical (7)
- Thoracic (12)
- Lumbar (5)
(Spinal cord ends at L1, conus medullaris begins at L2)
- Sacrum (5 - fused)
- Coccyx (4 - fused)

Beyond L2 are bundle of nerves called “cauda equina”

152
Q

Causes of spinal cord compression

A

Vertebral body neoplasms (thoracic most likely)
- disc herniation
- disc prolapse
- infection
- Trauma
- Spinal stenosis

153
Q

How do spinal cord lesions’ sensory and motor symptoms present

A

Motor - Contralaterally
Sensory - Ipsilaterally (same side)

154
Q

What nerve roots are implicated in knee jerk, big toe jerk and ankle jerk reflexes

A

Knee jerk - L3/4
Big toe - L5
Ankle - S1

155
Q

Signs/symptoms of spinal cord compression

A

Progressive (Hours-weeks/months) back pain and progressive leg weakness. Motor signs contralateral

UMN signs above level of lesion
LMN below level of lesion
Sensory loss 1-2 cord segments below lesion level
bladder/sphincter involvement is a late, bad signs

156
Q

What levels are the lesions in L5 nerve root compression and sciatica

A

L5 nerve root compression - L4/L5

Sciatica - L5/S1

157
Q

Specific causes of peripheral neuropathy

A

DAVID

Diabetes
Alcoholism
Vitamin B12 deficiency
Infective/inherited (GBS/Charcot-Marie-Tooth)
Drugs e.g. isonazid

158
Q

Define Brown Sequard syndrome

A

Damage to one half of the spinal cord, resulting in a specific pattern of symptoms:
- Ipsilateral motor weakness

  • Ipsilateral loss of proprioception (position sense), light touch, vibration at level of lesion
  • Contralateral loss of pain and temperature sense below level of lesion
159
Q

Gold investigation and management of Brown sequard

A

Investigations
- EMG (electromyography)
- MRI Spinal cord

Management
- Treatment of underlying condition
- High dose steroids

160
Q

Define/ explain pathophysiology of Charcot Marie Tooth syndrome

A

Group of inherited diseases (autosomal dominant) that cause axonal/myelin dysfunction. CMT1 and CMT2 most common

CMT 1 - loss of myelin sheath (onion bulb myelin due to schwann cell repair)
CMT 2 - Neuronal mitochondrial dysfunction = neurone death

Causes atrophy of muscle when motor neurones affected

161
Q

Signs/symptoms of charcot marie tooth

A

Weakness in lower legs and hands.
Loss of muscle tone and reflexes
Foot drop and claw hand
Tingling/burning in hands and feet
Thickened palpable nerves and hammer toes
“Inverted champagne bottle” legs due to distal muscle wasting

162
Q

Define Duchenne Muscular Dystrophy

A

X linked recessive condition characterised by severe muscle dystrophy due to absence of Dystrophin protein

163
Q

Signs/symptoms of duchenne muscular dystrophy

A

Usually presents 3-5 years.
- Weakness in pelvic muscles
- Waddling gait
- Gowers sign: due to inability to get up normally, they get into downward dog position then climb their hands up their legs to stand.
- Fat calves due to buildup of fat and fibrotic tissue rather than muscle

164
Q

Nerves implicated in wrist drop and claw hand

A

WD - Radial
Cl - Ulnar (4th and 5th fingers claw)

165
Q

What is Bells palsy

A

Acute, unilateral, idiopathic facial nerve paralysis.

Aetiology unknown, but suspected HSV

166
Q

How does Bells palsy present

A

LMN Facial nerve palsy -> Forehead affected
(UMN spares upper face)
- Post auricular pain
- Altered taste
- Dry eyes
- Hyperacusis

167
Q

How is Bell’s palsy treated

A

Prednisolone within 72 hours, maybe add antiviral

most people with Bell’s palsy make a full recovery within 3-4 months

168
Q

What is temporal arteritis

A

AKA Giant cell arteritis. Branches of carotid artery (

Occurs in >50, usually ~70. Strong association with Polymyalgia Rheumatica.

Early recognition and treatment can minimise risk of complications e.g. permanent sight loss.

169
Q

How does temporal arteritis present

A
  • Rapid <1 month onset
  • Unilateral headache around temple/forehead
  • Diminished/absent temporal artery
  • Jaw claudication
  • Blurred/double vision
  • Optic disc pallor
  • Scalp tenderness (Painful to comb)
  • Fever, muscle aches, weight loss, loss of appetite
170
Q

GCA typical presentation

A

50+ white female with unilateral temple headache, scalp tenderness (painful to comb), jaw claudication and vision changes.

171
Q

Pathophys of GCA

A

Granulomatous vasculitis of large/medium arteries. Arteries become inflamed, intima is thickened and vascular lumen is narrowed. Usually cerebral (temporal) arteries affected:
- Superficial temporal artery: Headache/scalp tenderness
- Mandibular artery: jaw claudication
- Ophthalmic artery: visual loss (retinal ischaemia)

172
Q

Diagnostic criteria in GCA

A

3 of:
- Over 50
- New headache
- Temporal artery tenderness/diminished pulse
- ESR Raised
- Abnormal temporal artery biopsy

173
Q

Management of GCA

A

High dose prednisolone

  • Sight loss (amaurosis fugax!)
    Should be dealt with ASAP or could lead to permanent blindness
  • Ischaemic cranial complications (Visual loss/stroke)
  • Aortic aneurysm
174
Q

In cases where long term steroids are given, what 2 systems should be protected and how is this done?

A

GI (stomach and oesophagus) and Bones
- PPI (omeprazole)
- Alendronate (bisphosphonate)
- Ca2+ and vitamin D

175
Q

Define polymyalgia rheumatica

A

Condition that causes pain stiffness and inflammation in neck, shoulders and hips. Limits range of motion. Occurs alongside GCA often.

Morning pain/stiffness in shoulders etc. Leads to fatigue, fever, weight loss, anorexia and depression

Raised ESR but CK and EMG normal

Managed with prednisolone

176
Q
A

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