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Phase 2a Gold Standard > Neuro > Flashcards

Neuro Flashcards

1
Q

Explain the anterior and posterior circulation of the Circle of Willis

A

Anterior - branches of internal carotid
- Anterior Choroidal artery
- Anterior/Middle cerebral artery

Posterior - branches of vertebrobasilar arteries
- Posterior Cerebral artery
- Basilar artery
- Superior cerebellar artery
- Anterior/Posterior inferior cerebellar artery

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2
Q

What is Broca’s area, and what does an injury of it cause?

A

Located in the frontal lobe of person’s dominant side (left in right handed people) and influences motor production of speech.

Causes expressive aphasia - Patients can understand speech but can’t produce it themselves

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3
Q

What is Wernickes area and what does injury of it cause

A

Located in parietal and temporal lobe of person’s dominant side (left in right handed people) , influences understanding of speech and using correct words to express thoughts

Causes receptive aphasia - Patients can produce speech but don’t understand the meaning of spoken words

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4
Q

What are Wernickes and Brocas areas supplied by?

A

Middle Cerebral Artery

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5
Q

What is a watershed area?

A

Areas furthest from blood supply, most susceptible to infarction

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6
Q

Define ischaemic stroke

A

Reduced cerebral blood flow due to arterial occlusion or stenosis. Account for 85% of all strokes.

Consists of rapidly developing signs of cerebral dysfunction, lasting more than 24 hours, with no apparent cause.

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7
Q

Causes of ischaemic stroke

A

Disruption of blood supply secondary to:
- Thrombus formation/ embolus
- Atherosclerosis
- Shock
- Vasculitis
- Hypercoagulability (thrombophilia)

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8
Q

Risk factors for stroke (9)

A
  • Male
  • Old (>55)
  • Black or Asian
  • History of Ischaemic stroke or TIA
  • Atrial fibrillation
  • Sickle cell disease
  • Combined contraceptive pill
  • Carotid artery stenosis
  • Smoking, obesity, HTN, T2DM
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9
Q

Define hemiparesis

A

Weakness or paralysis on one side of the body

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10
Q

Manifestations of an Anterior Cerebral Artery ischaemic stroke

A
  • Contralateral hemiparesis and sensory loss, affecting lower limbs>upper limbs
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11
Q

Manifestations of middle cerebral artery stroke

A
  • Contralateral hemiparesis and sensory loss affecting upper limbs>lower limbs.
  • Aphasia if affecting Broca or Wernickes areas in dominant hemisphere
  • Homonymous hemianopia (visual field defect in same side of both eyes)
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12
Q

Manifestations of Posterior Cerebral Artery stroke

A
  • Contralateral homonymous hemianopia with macular sparing (preservation of central visual field)
  • Contralateral loss of pain and temperature
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13
Q

Manifestations of Vertebrobasilar artery stroke

A

Cerebellar signs (intention tremor, nystagmus, hypotonia)
Reduced consciousness
Quadriplegia

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14
Q

Manifestations of Webers syndrome (midbrain infarct)

A

Oculomotor palsy and contralateral hemiplegia

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15
Q

Manifestations of Lateral medullary syndrome (posterior inferior cerebellar artery occlusion)

A

Ipsilateral facial loss of pain and temperature
Ipsilateral Horner’s syndrome: miosis, ptosis, anhidrosis
Ipsilateral cerebellar signs
Contralateral loss of pain and temperature

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16
Q

What is lacunar stroke?

A

Stroke affecting small branches of middle cerebral artery.

Causes one of the following:
Pure motor loss
pure sensory loss,
ataxic hemiparesis

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17
Q

What is pronator drift

A

Ask patient to raise arms. On the affected side, palm and arm will face inward and downwards. Suggests muscle weakness.

(Symptoms contralateral to affected brain side)

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18
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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19
Q

Investigations on stroke presentation

A
  • Assessment using ROSIER scale
    (stroke possible if >0)
  • Non contrast CT head (rule out haemorrhagic stroke)
  • CT Angiogram (identify occlusion - hypoattenuation of brain parenchyma, loss of matter differentiation)
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20
Q

How do strokes appear on CT

A

Ischaemic - Darkness of brain parenchyma
Haemorrhagic - Brightness surrounded by darkness (blood surrounded by oedema)

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21
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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22
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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23
Q

What classification system is used in stroke?

A

Bamford classification - categorises stroke based on area of circulation affected.

  • Total anterior circulation stroke - Anterior/middle cerebral artery (all 3 - Unilateral weakness of face,arm or leg, homonymous hemianopia, higher cerebral dysfunction)
  • Partial anterior circulation stroke - only part of anterior circulation (2 out of 3 symptoms)
  • Lacunar - Either: All sensory, all motor or ataxic hemiparesis
  • Posterior circulation syndrome (1 of cranial nerve palsy, bilateral motor/sensory defecit, eye movement disorder, homonymous hemianopia)
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24
Q

Scoring system for risk of stroke after Atrial Fibrillation

A

CHA2DS2 VASc

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25
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

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26
Q

Symptoms of TIA

A
  • Contralateral numbness, face drooping, dysphasia, vision loss
  • Amaurosis Fugax

Same as stroke but lasts less than 24 hours and no lasting effects

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27
Q

What acronym helps identify stroke in public

A

FAST
Face
Arms
Speech
Time

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28
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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29
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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30
Q

Management of TIA

A

1st line - 300mg Aspirin daily for 2 weeks
- Clopidogrel daily long term
- Atorvastatin

ABCD2 score to assess stroke risk

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31
Q

What is it called when 2 TIAs happen in close proximity

A

Crescendo TIAs.
Requires urgent referral

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32
Q

What are the layers over the brain called

A

Meninges of the brain

  • Dura mater
  • Arachnoid
  • Pia mater (innermost layer)
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33
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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34
Q

Risk factors for haemorrhagic stroke (6)

A

Head injury
Hypertension
Aneurysms
Brain tumour
Connective tissue disorder
Family history

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35
Q

General symptoms of haemorrhagic stroke

A

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

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36
Q

Give the scoring system for unconsciousness

A

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

Minimum score 1 per category

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37
Q

Give the scoring system for consciousness

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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38
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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39
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

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40
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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41
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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42
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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43
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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44
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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45
Q

Define acute acute on chronic and chronic subdural haemorrhage

A

Acute - symptoms <2 days since injury
Acute on chronic - 3-14 days
Chronic - >15 days

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46
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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47
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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48
Q

What GCS score requires intubation

A

8 or below

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49
Q

Specific surgical management used in subdural haemorrhage

A

Burrhole washout if haemorrhage small

Craniotomy if large haemorrhage

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50
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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51
Q

Other causes of subarachnoid haemorrhage

A
  • Trauma
  • AV malformations
  • Vasculitis
  • Bleeding disorders
  • Brain tumour bleeding
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52
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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53
Q

Pathophysiology of subarachnoid haemorrhage

A
  • Berry aneurysm rupture causes bleeding into subarachnoid space, increasing ICP, which puts pressure on nearby tissue and blood vessels, causing tissue infarction
  • Blood vessels bathing in pool of blood vasospasm. If this affects circle of Willis, further ischaemic damage to brain
  • Blood irritates meninges, causing inflammation/scarring of surrounding tissue (meningism symptoms). Scar tissue obstructs normal outflow of CSF, causing buildup known as hydrocephalus
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54
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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55
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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56
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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57
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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58
Q

CT Appearance in subarachnoid haemorrhage

A
  • Blood in subarachnoid space (hyperdense)
  • Star shaped lesion (blood filling in gyro pattern)
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59
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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60
Q

Define intracerebral haemorrhage with causes

A

Bleeding directly into brain tissue. Presents the same as ischaemic stroke.

Can occur spontaneously, due to ischaemic infarct, tumour or aneurysm rupture

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61
Q

Treatment options for intracerebral haemorrhage

A

Surgical:
- Craniotomy (if close to surface)
- Stereotactic aspiration (aspirate blood, relieve ICP)

IV Mannitol for ICP

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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

Why is group B strep common in neonatal meningitis

A

Because group B strep lives harmlessly in the maternal vagina

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66
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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67
Q

Pathophysiology of meningitis

A

Infection of leptomeninges and CSF. Infection route via direct spread or haematogenous spread. WBC. Causes white blood cell infiltration of CSF (>5 diagnostic). Bacterial and viral cause increase in protein. Bacterial causes decrease in glucose and forms pus.

Fungal infection can cause chronic meningitis.

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68
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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69
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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70
Q

Fungal appearance of CSF in meningitis

A

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

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71
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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72
Q

Management of viral meningitis

A

Supportive (Analgesia, hydration etc)
Aciclovir

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73
Q

Complications of meningitis

A

Hearing loss
Seizures
Cognitive impairment
Hydrocephalus
Sepsis

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74
Q

Define Encephalitis

A

Inflammation of brain parenchyma, mostly frontal and temporal lobes.

Usually viral cause but can be autoimmune

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75
Q

Causes and epidemiology of encephalitis

A

Usually in elderly or babies, or immunosuppressed
Infective
- Infective: Herpes simplex virus (HSV-1 - Cold sores, HSV-2 genital herpes)
- N meningitidis
- TB

Non infective: Autoimmunity

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76
Q

Signs/symptoms of encephalitis

A

Triad:
- Fever, headache, altered mental status
Meningism:
- Stiff neck, headache, photophobia

Also presents with neurological deficit
- Aphasia/Dysphasia

  • Hemiparesis
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77
Q

Investigations in encephalitis

A

FBC - high WCCs (infection)
ESR/CRP raised

Lumbar puncture - high lymphocytes
Throat swab for viral culture

CT/MRI head GOLD (Areas of inflammation in brain)

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78
Q

Management of encephalitis

A

Urgent hospital admission and aciclovir

(Ganciclovir if cytomegalovirus)

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79
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)

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80
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.

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81
Q

Risk factors for multiple sclerosis (6)

A

Female
20-40
Vitamin D deficiency
Family history (HLA-DR2)
Autoimmunity
EBV infection

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82
Q

Pathophysiology of multiple sclerosis

A

T cells cross Blood Brain Barrier and launch immune response against oligodendrocytes. Eventually, plaques form.

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

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83
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
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84
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.

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85
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

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86
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)

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87
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

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88
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

89
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

90
Q

Management of complications of MS (4)

A
  • Spasticity - Baclofen and gabapentin
  • Neuropathic pain/depression - amitriptyline
  • Physiotherapy for spasticity and mobility impairment
91
Q

Other complications of MS

A

UTI
Constipation
Visual impairment
Erectile dysfunction

92
Q

Define Huntington’s disease

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)

93
Q

Pathophysiology of Huntington’s disease

A

CAG (glutamine) repeats >36x in HTT gene on chromosome 4. Mutated Huntingtin proteins aggregate within neuronal cells of caudate and putamen. This causes cell death of GABAergic and cholinergic neurones, causing ACh and GABA deficiency, so less dopamine inhibition. Excess dopamine causes excessive thalamic stimulation so excess movement.

Also displays “genetic anticipation”. The more copies of the protein DNA polymerase adds on in the sperm, the earlier the onset and the more severe the disease.

94
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

95
Q

Investigations in Huntington’s

A
  • Clinical diagnosis
  • Genetic testing GOLD

CT/MRI
- Caudate and striatal atrophy
- Increased size of lateral ventricles

96
Q

Other causes of chorea

A

Hyperthyroid
Wilson’s
SLE
Dementia

97
Q

Management of Huntington’s

A

Uncurable

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

98
Q

Define Parkinson’s disease

A

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

99
Q

Pathophysiology of Parkinson’s disease

A

Loss of dopaminergic neurones in Substantia Nigra. Misfolded a-synuclein proteins called Lewy bodies are also present histologically (show as dark eosinophilic inclusions)

This causes a dopamine deficiency

100
Q

What are the “parkinsonism” symptoms

A

Resting Tremor
Bradykinesia
Rigidity
Postural instability

101
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

102
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
103
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 (stop breakdown of circulating dopamine)
- Selegiline

104
Q

Why should Levodopas only be used in severe Parkinson’s

A

The body becomes resistant to the effects of it overtime and effects begin to wear off. This leads to “on and off” periods where motor function fluctuates between being well controlled and suddenly declining

105
Q

Complications of Parkinson’s

A
  • Disease progression and motor fluctuations (off periods when treatment stops working)
  • Freezing (sudden stop of movement)
  • Dyskinesia
  • Dementia
106
Q

Differentials of Parkinsonism

A

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

107
Q

Define Myasthenia Gravis

A

Type 2 hypersensitivity reaction causing autoimmune destruction of the post synaptic membrane at the neuromuscular junction of skeletal muscle.

Mostly affects facial muscles.

Strong association with thymoma/ thymic hyperplasia

108
Q

Pathophysiology of Myasthenia Gravis

A

Nicotinic Acetylcholine Receptor antibodies (Anti-AChR) bind to ACh binding sites at post synaptic membrane, competitively inhibiting ACh binding, causing less effective muscle contraction. Binding increases with exertion, increasing the severity of symptoms with increased activity, and showing improvement at rest.

Antibodies also activate the complement system, damaging the post synaptic membrane.

Some patients also have anti muscle-specific kinase (Anti-MuSK) and anti low-density lipoprotein receptor-related protein 4 (anti-LRP4) antibodies, leading to inadequate ACh receptor production.

109
Q

Epidemiology of myasthenia gravis

A

20-30 for females
60-70 for males

110
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)

111
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

112
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

113
Q

Explain the main differential of Myasthenia gravis

Cause
Association
Symptoms
Treatment

A

Lambert Eaton syndrome

  • Caused by autoimmunity against presynaptic voltage gated Ca2+ channels, meaning enough ACh isn’t released
  • Associated with Small Cell Lung cancer
  • Symptoms improve with exercise/exertion
  • Symptoms start at extremities and spread to head and neck. Also dry eyes and mouth due to autonomic dysfunction
  • Treated with Steroids and IV immunoglobulins
114
Q

Management of Myasthenia Gravis

A

Acetylcholinesterase inhibitor - Pyridostigmine
Prednisolone (immunosuppression)

Surgical: Thymectomy

115
Q

What is the main complication of Myasthenia Gravis

A

Myasthenic Crisis - Weakening of respiratory muscles, usually provoked by infection or medication. Presents as sudden shortness of breath and can lead to respiratory failure

116
Q

Treatment of myasthenic crisis

A

Ventilation
Non invasive - BiPAP
Full intubation and ventilation if severe

+ IV immunoglobulins or plasma exchange

117
Q

Define Guillain Barre Syndrome

A

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

Acute, symmetrical, ascending weakness!

118
Q

Causative infective pathogens of Guillain Barre syndrome

A

Bacteria:
- Campylobacter Jejuni
- M. pneumoniae

Viral:
- Cytomegalovirus
- EBV

119
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
120
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.

121
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)
122
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

123
Q

Management of Guillain barre syndrome (2 + 2 for complications)

A

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

VTE Prophylaxis (LMWH)
Ventilation if low FVC

124
Q

Complications of GBS

A

Respiratory failure
PE
DVT
Autonomic dysfunction

125
Q

Upper motor neurone lesion area

A

Anywhere from pre central gyrus to anterior spinal cord

126
Q

Lower motor neurone lesion area

A

Anywhere from Anterior spinal cord to innervated muscle

127
Q

How is muscle power affected in upper motor neurone lesions?

A

In arms flexors>extensors
In legs extensors>flexors

128
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

129
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 - Up
Spastic paralysis
Hyperreflexia
No fasciculations
Babinski positive
Voluntary movement slowed
Muscle tone and power kept

LMN - Down
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)

130
Q

Risk factors for MND

A

Family history (SOD1 mutation)
Smoking
Exposure to heavy metals and pesticides
Male

131
Q

Define Motor Neurone Disease

A

Cluster of neurodegenerative diseases characterised by axonal degeneration of ONLY MOTOR neurones in motor cortex, cranial nerve nuclei and anterior horn of spinal cord

132
Q

Subtypes of MND

A

Amyotrophic Lateral Sclerosis (ALS) - Most common
- UMN and LMN
- SOD1 association

Primary Lateral Sclerosis - UMN only

Progressive Muscular Atrophy (PMA) - LMN only
- Distal muscles before proximal (e.g. clumsy hands)

Progressive Bulbar Palsy (PBP) - LMN only
- Primarily affects talking and swallowing muscles

133
Q

Pathophysiology of MND (5)

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
134
Q

Signs and symptoms of MND (4)

A

Mixed UMN and LMN signs
Muscle wasting
Dysarthria and dysphagia
Split hand sign in ALS

135
Q

Investigations of MND (3)

A

Clinical diagnosis - El Escorial criteria
LMN and UMN signs in 3+ regions diagnoses ALS

Electromyography assesses health of muscles and motor neurones

MRI brain/ lumbar puncture to rule out other causative pathology e.g. spinal cord compression

136
Q

Management of MND (2)

A

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

137
Q

Complications of MND

A

Respiratory failure
Aspiration pneumonia (usually kills within 3 years of symptom onset)

138
Q

What MDT help may be needed in MND (3)

A

Speech/language therapy
Physiotherapy
Palliative care

139
Q

Define dementia

A

Syndrome caused by a number of brain disorders (e.g. Alzheimers) causing memory loss, difficulties thinking, problem solving, language and every day thinking

140
Q

Risk factors for Alzheimers

A

Increasing age
Genetics
Family history
Downs
Female

141
Q

Define Alzheimers

A

Most common form of dementia. Progressive neurodegeneration in mental performance due to neuronal cell death

142
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
143
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)
144
Q

Pathophysiology of Alzheimer’s

A

Senile beta amyloid plaques:
Beta amyloid proteins stick together forming Senile plaques. These get between neurones, block signalling and trigger inflammation. Also deposit in blood vessels around brain, weakening walls.

Neurofibrillary tangles:
Tau proteins found in neurone cytoskeleton become hyperphosphorylated, causing them to change shape and tangle, inhibiting signalling and causing apoptosis of neurones. Brain atrophies due to neurone death.

145
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
146
Q

How would Alzheimers affect behaviour (4)

A

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

147
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)

148
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

149
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)

150
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.

151
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)

152
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.

153
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

154
Q

Management of Lewy Body Dementia

A

Dopamine analogue - Levodopa
ACh-esterase inhibitor - Donepezil

155
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.

156
Q

Genetic causes of frontotemporal dementia

A

Microtubule associated protein tau (chromosome 17)
Granulin precursor (chromosome 17)

157
Q

Pathophysiology of frontotemporal dementia

A

3R isoform of Tau protein becomes hyperphosphorylated and forms tangles. 3R tau tangles are called Pick Bodies. When these apoptose, it causes brain atrophy in frontotemporal lobes but also ventricles expand.

(as opposed to 3R+4R neurofibrillary tangles in Alzheimer’s)

158
Q

Signs and symptoms of frontotemporal dementia

A

Frontal
- Disinhibition
- Loss of empathy
- Apathy
- Compulsive behaviour

Temporal
- Difficult speech/ataxia
- Speech sound errors

Leads to memory loss, lack of concentration, inability to learn

159
Q

Diagnosis and management of frontotemporal dementia

A
  • Cognitive assessment diagnostic
  • MRI shows frontal and temporal lobe atrophy
  • Incurable, SSRI (citalopram) and donepezil used to aid symptoms
160
Q

Give Primary and secondary causes of headache

A

Primary
- Migraine
- Tension
- Cluster

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

161
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)

162
Q

Common migraine triggers

A

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

163
Q

5 stages of migraine

A
  • Prodrome (irritability, depression, fatigue) (Days-hours before migraine)
  • Aura (Strange smells, hallucinations (zigzag lines classic), photophobia) (~60mins before onset)
  • Headache (lasts 4-72 hrs)
  • Resolution
  • Postdrome/recovery phase

(Migraine can present without Aura)

164
Q

Pathophysiology of migraine

A

In aura: Serotonin increases (vasoconstriction), then decreases beyond normal (vasodilation)

In migraine: Cortical spreading depression causes brain to become hypersensitive to certain stimuli. Causes inflammation of CN5 nucleus and meningeal blood vessel dilation.

165
Q

Signs/symptoms of Migraine

A

Moderate/severe unilateral pulsating headache that is aggravated by routine activity, lasts up to 72 hours
(usually uni but can be bilateral! - Don’t get caught out)

Associated with:
- Photophobia/ Phonophobia
- Nausea/vomiting

166
Q

Signs/symptoms of 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

167
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

168
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

169
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

170
Q

Risk factors/causes of tension headache

A

Stress
Eye strain
Depression
Skipping meals
Dehydration
Sleep deprivation
Noise

171
Q

Signs/symptoms and management of tension headache

A

Bilateral
Pressing/tight (“Tight band”)
Mild/moderate pain
Lasts mins-hours
May radiate to neck

Managed with basic analgesia (Paracetamol/NSAID/aspirin)

172
Q

Why should opiates be avoided?

A

To avoid dependence

173
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

174
Q

Signs/symptoms of cluster headache

A

Severe unilateral, periorbital, crescendo headache, lasting 15mins to 3 hours.
(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

175
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

176
Q

Define trigeminal neuralgia

A

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

177
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.

178
Q

Common triggers of trigeminal neuralgia pain

A
  • Light touch (washing, shaving, brushing teeth)
  • Talking
  • Cold weather
  • Spicy food
  • Caffeine and citrus
179
Q

What are the branches of the trigeminal nerve

A

Ophthalmic
Maxillary
Mandibular

180
Q

Signs/symptoms of trigeminal neuralgia

A

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

181
Q

Investigations and management of trigeminal neuralgia

A

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

Carbamazepine first line
Surgery (microvascular decompression)

182
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

183
Q

Causes of cauda equina

A
  • Lumbar disc herniation (L4/L5 or L5/S1)
  • Trauma
  • Lumbar spinal stenosis (secondary to spondylitis, rheumatoid arthritis etc)
184
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.
185
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
186
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”

187
Q

Causes of spinal cord compression

A
  • Vertebral body neoplasms (thoracic most likely)
  • Disc herniation
  • Disc prolapse
  • Infection
  • Trauma
  • Spinal stenosis
188
Q

How do spinal cord lesions’ sensory and motor symptoms present

A

Motor - Contralaterally
Sensory - Ipsilaterally (same side)

189
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

190
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
191
Q

Investigation and management in spinal cord compression

A

Urgent MRI spine

Surgical decompression (laminectomy or microdiscectomy)

192
Q

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

A

L5 nerve root compression - L4/L5

Sciatica - L5/S1

193
Q

Causes of nerve malfunction

A
  • Demyelination (GBS)
  • Axonal degeneration
  • Compression
  • Infarction
  • Infiltration (by inflammatory cells (leprosy) or neoplastic cells)
  • Trauma causing Wallerian degeneration (distal death)
194
Q

Specific causes of peripheral neuropathy

A

DAVID

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

195
Q

signs and symptoms of peripheral neuropathy

A

Numbness and tingling of feet or hands
Burning, stabbing, shooting pain in affected areas
Loss of balance/coordination
Muscle weakness, esp feet

196
Q

Causes of mononeuritis multiplex

A

(several individually affected nerves at once)
WARDS PLC
Wegeners/vasculitis
AIDS/Amyloidosis
Rheumatoid Arthritis
DMT2
Sarcoidosis
Polyarteritis nodosa
Leprosy
Carcinomas

197
Q

Define carpal tunnel syndrome

A

A collection of symptoms caused by compression of the median nerve in the carpal tunnel. The median nerve originates from nerve roots C6-T1. Only affects first 4 fingers (including thumb). Palm may be spared as it is innervated by superficial palmar branch of medial nerve that is upstream of carpal tunnel.

Little finger and proximal side of ring finger innervated by ulnar nerve so are spared. Back of hand innervated by radial nerve.

198
Q

Signs/symptoms of carpal tunnel syndrome

A
  • Pain worse at night, after days use
  • Paraesthesia (relieved by hanging over bed and shaking “wake and shake”)
  • Muscle weakness especially in fingers
  • Tinels, Phalans, Durkans positive on examination
199
Q

Explain Tinel’, Phalen’s, Durkans signs

A

Phalen’s - flex wrist as far forwards as possible and hold for a minute. Causes numbness in median nerve areas.

Tinel’s - tap transverse carpal ligament, reproduces tingling/ pins and needles in areas of median nerve.

Durkan’s - Manually compressing carpal tunnel causes signs of CPS

200
Q

What are possible causes of carpal tunnel syndrome

A

Repetitive stress injury
Obesity
Diabetic neuropathy
Acromegaly
Neoplasms
Amyloidosis

201
Q

Gold investigation and treatment of carpal tunnel

A

Electromyography confirms lesion site and severity

Night time wrist splint and steroid injection

202
Q

Define sciatica with symptoms, investigation and treatment

A
  • L5/S1 lesion
  • Pain/numbness from buttock down lateral leg to pinky toe. Weak plantar reflex and absent ankle jerk.
  • Examination: Cant raise straight leg without pain
  • Treated with basic analgesia and physiotherapy. Surgery if severe
203
Q

Define Brown Sequard syndrome

A

Damage to one half of the spinal cord, resulting in a specific pattern of symptoms

204
Q

Signs of brown sequard syndrome

A

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

205
Q

Gold investigation and management of Brown sequard

A

Investigations
- EMG (electromyography)
- MRI Spinal cord

Management
- Treatment of underlying condition
- High dose steroids

206
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

207
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
208
Q

Define Duchenne Muscular Dystrophy

A

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

209
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

210
Q

Nerve implicated in wrist drop

A

Radial Nerve

211
Q

Nerve implicated in Claw hand

A

Ulnar nerve (4th and 5th finger claw)

212
Q

Nerve usually implicated in foot drop, and other causes

A

Peroneal nerve (foot dorsiflexion)

Other causes:
- Muscular dystrophy
- Spinal cord/brain injury
- Peripheral neuropathy due to diabetes
- Trauma

213
Q

Where do brain cancers normally metastasise from

A

NSCLC (MC) and SCLC
Breast cancer
Melanoma
RCC
Gastric cancer

214
Q

What is the most common brain cancer

A

Gliomas (tumour of glial cells) of which astrocytoma is most malignant (e.g. Glioblastoma multiforme)
- Has pseudo-palisading pattern histologically
- Grade IV

215
Q

How are brain cancers graded

A

Using WHO’s scale. IV most malignant

216
Q

Symptoms of Cerebellar involvement in brain cancer

A

DASHING
Dysdiadokinesis
Ataxia
Slurred speed (dysarthria)
Hypotonia
Intention tremor
Nystagmus (remember Charcot’s Neurological Triad!)
Gait abnormality

217
Q

General signs and symptoms of brain cancer

A

Weight loss
Cushings triad (increased pulse pressure, bradycardia, irregular breathing)
Increased ICP
Seizures

218
Q

Investigations in brain cancer

A

MRI and then biopsy to grade tumour.

Lumbar puncture contraindicated

Phase 2a Gold Standard (29 decks)

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