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Medicine Phase 2A (OWN) > Neurology > Flashcards

Neurology Flashcards

1
Q

Describe the main functions of the brain lobes, cerebellum and brainstem

A

Frontal: movement and executive function
Parietal: sensory
Temporal: hearing, smell, memory, languages, facial recognition
Occipital: vision
Cerebellum: muscle coordination, balance
Brainstem: HR, BP, breathing, GI function, consciousness

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2
Q

Which parts of the brain are supplied by the anterior cerebral artery?

A

Medial frontal and parietal

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3
Q

Which parts of the brain are supplied by the posterior cerebral artery?

A

Mainly occipital, some temporal and thalamus

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4
Q

Which parts of the brain are supplied by the middle cerebral artery?

A

Lateral portions of the frontal, temporal and parietal lobes

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5
Q

Where are the most common sites for atherosclerosis in the brain?

A

Branch points, particularly of the internal carotid and middle cerebral

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6
Q

Describe a lacunar stroke and it’s causes

A

Hyaline arteriosclerosis of the deep MCA branches leads to protein-filled cyst formation in the brain
Caused by HTN and diabetes

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7
Q

What is a watershed infarct?

A

Area of the brain damaged that is at the border of two blood supplies

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8
Q

How does cytotoxic oedema occur as a result of an ischaemic stroke?

A

No glucose and oxygen so no energy

High sodium and calcium in the cells draws water in via osmosis

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9
Q

How do high calcium levels in the brain cells cause damage in an ischaemic stroke?

A

High Ca2+ causes a buildup of ROS which damage lipids in the mitochondria and lysosomes
Release of apoptosis-releasing factors and digestive enzymes

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10
Q

What is the major risk if inflammation damages the blood-brain barrier in an ischaemic stroke?

A

Vasogenic oedema which has a mass effect and pushes into the other side, can causes cingulate/ uncle herniation
If cerebellar tonsil herniation it may compress the brainstem causing breathing problems and reduced consciousness

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11
Q

Give two symptoms of an anterior/ middle cerebral artery ischaemia

A

Numbness

Muscle weakness

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12
Q

How would an ischaemic stroke affecting Broca’s area present?

A

Slurred speech

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13
Q

How would an ischaemic stroke affecting Wernicke’s areas present?

A

Difficulty understanding speech

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14
Q

How would you diagnose an ischaemic stroke?

A

Flair MRI
CT scan
Angiography

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15
Q

How would you treat an ischaemic stroke?

A

Thrombolytic enzymes: tissue plasminogen activator (TPA)
Aspirin: prevents more clots
Surgery: mechanical embolus removal in cerebral ischaemia (MERCI)
Suction removal

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16
Q

How could you minimise risk factors of an ischaemic stroke?

A 
Quit smoking
Healthy BP
Normal cholesterol
Control of diabetes
Surgery
Carotid endarterectomy
Stent
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17
Q

How can HTN cause an intracerebral haemorrhage?

A 
Micro aneurysms (Charcot-Bouchard aneurysms)
Hyaline arteriolosclerosis (arteries are still and more likely to rupture)
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18
Q

Give 4 conditions associated with intracerebral haemorrhage

A

Arteriovenous malformations
Vasculitis
Vascular tumours
Cerebral amyloid angiopathy (protein deposits in the walls of arterioles making them less compliant)

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19
Q

How can an intracerebral haemorrhage occur as a result of ischaemic stroke?

A

Brain tissue death due to ischaemia, if there is reperfusion damaged cells may rupture causing a haemorrhage / haemorrhagic conversion (bleeding into dead tissue)

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20
Q

Where might herniation occur in an intracerebral haemorrhage?

A

Falx cerebri
Tentorium cerebelli
Foramen magnum

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21
Q

How would you treat an intracerebral haemorrhage?

A

Medication: anti-hypertensives and to relieve ICP
Surgery: craniotomy (relieving ICP and draining blood)
Sterotatic aspiration (CT and needle)

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22
Q

Where is CSF found within the meninges?

A

Subarachnoid space

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23
Q

Give 3 causes of a subarachnoid haemorrhage

A

Traumatic injury

Aneurysms (saccular cerebral/ berry aneurysms)
Genetic disorders: Marfan syndrome can predispose people
Can rupture with increased ICP

Arteriovenous malformation

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24
Q

Describe the consequences of a subarachnoid haemorrhage

A

Pressure on the skull, brain tissue and blood vessels

Arteries bathing in a pool of blood can start to intermittently vasoconstrict/ vasospasm
In circle of Willis there is reduced blood to the brain

Blood irritates the meninges causing inflammation and scarring of surrounding tissue, this can obstruct CSF and cause dilation of the ventricles (hydrocephalus) which increases ICP

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25
Q

Give 4 symptoms of a subarachnoid haemorrhage

A 
Thunderclap headache
Nuchal rigidity
Seizures
Vomiting
Vision changes
Confusion
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26
Q

How would you diagnose a subarachnid haemorrhage?

A

CT
MRI
Lumbar puncture (red blood: fresh/ yellowish blood (bilirubin): old)

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27
Q

How would you treat a subarachnoid haemorrhage?

A

Emergency surgery: clip artery and apply pressure
Use catheter to insert coil to promote clot formation
Medication: CCB to prevent vasospasms

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28
Q

Give the diagnostic criteria for a TIA

A

<24 hours of symptoms, no evidence of infarct on imaging

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29
Q

Describe an extra/ epidural haemorrhage

A

Bleeding that occurs between the skull and dura mater

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30
Q

Give 4 causes of an epidural haemorrhage

A

Trauma
Motor vehicle accident
Falls
Assault

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31
Q

What percentage of epidural haemorrhages include a skull fracture?

A

70-95%

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32
Q

Describe the clinical manifestation of an epidural haemorrhage

A 
Altered consciousness
Headache
Vomiting
Confusion/ seizures
Aphasia
Pupil asymmetry
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33
Q

How would you diagnose an epidural haemorrhage?

A

CT/ MRI:lens shaped lesion, well circumscribes

X-ray: may show fractures of the skull

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34
Q

Which investigation is contraindicated in an epidural haemorrhage?

A

Lumbar puncture

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35
Q

How would you treat an epidural haemorrhage?

A

Urgent decompression
ABCD, high flow oxygen
Sit up in bed
Neurosurgery: blood is evacuated

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36
Q

Describe epilepsy

A

Recurring and unpredictable seizures, neutrons are synchronously active

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37
Q

Give the main excitatory neurotransmitter in the brain and the primary receptor

A

Glutamate

NMDA (Ca2+ enters)

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38
Q

Give the main inhibitory neurotransmitter in the brain and the primary receptor

A 
GABA
GABA receptor (Cl- enters)
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39
Q

Give 3 ways in which the excitatory and inhibitory receptors in the brain can be affected

A

Tumours
Brain injury
Infection

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40
Q

Describe a focal seizure without impaired awareness

A

One hemisphere/ lobe affected
Strange sensations, jerking movements
Jacksonian march: starts in one group, spreads
Awake/ alert, often remembers

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41
Q

Describe a focal seizure with impaired awareness

A

Focal seizure with loss of awareness or responsiveness

May not remember

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42
Q 
Describe the following generalised seizures:
Tonic
Atonic
Clonic
Tonic-clonic
Myoclonic
Absence
A 
Stiff/ flexed, fall back
Relaxed, fall forward
Convulsions
2 phases
Short muscle twitches
"Spaced-out"
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43
Q

Describe status epilepticus

A

If seizure lasts longer than 5 minutes, is ongoing/ without returning to normal (usually tonic-clonic)
Often treated with benzodiazepines which enhance GABA

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44
Q

Give 2 main post-seizure symptoms

A

Postictal confusion
Paralysis (Todd’s paralysis: arms and legs)
Lasts around 15 hours, temporary and severe suppression of seizure-affected brain area

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45
Q

How would you diagnose epilepsy?

A

Imaging to look for abnormalities (MRI, CT)

EEG

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46
Q

How would you treat epilepsy?

A 
Daily medication:
Anticonvulsants
Epilepsy surgery- remove cause
Vagus nerve stimulation
Ketogenic diet
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47
Q

Describe Parkinson’s disease

A

Degeneration of dopamine-producing neutrons of the substantia nigra causing a progressive movement disorder

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48
Q

Give the two genes in which a mutation may cause Parkinson’s

A

PINK1, PARKIN

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49
Q

Give 2 risk factors for Parkinson’s

A

Pesticide exposure

Genetic variants

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50
Q

Describe the substantia nigra and it’s function

A

Part of basal ganglia that connects to the motor cortex and controls movement

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51
Q

What is the feature found in neutrons before they die in Parkinson’s disease?

A

Lewy bodies (eosinophilic, alpha-synuclein)

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52
Q

Which part of the substantia nigra is affected in Parkinson’s disease?

A

Pars compacta

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53
Q

What does the nigrostriatal pathway connect and what is it’s purpose?

A

Substantia nigra to striatum (caudate and putamen)

Helps stimulate cerebral cortex to initiate movement

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54
Q

Describe the motor clinical features of Parkinson’s

A

Resting tremor
Rigidity, stooped posture, almost expressionless
Postural instability
Bradykinesia, hypokinesia, akinesia (difficulty initiating movement) : legs freeze up, shuffling gait

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55
Q

How does Parkinson’s differ from motor cortex/ corticospinal pathway diseases?

A

No weakness in Parkinson’s

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56
Q

Give 4 non-motor symptoms of Parkinson’s

A

Depression
Dementia
Sleep disturbances
Difficulty smelling

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57
Q

Why can Parkinson’s not be treated with dopamine?

A

Dopamine cannot cross the blood-brain barrier

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58
Q

What would the first line of Parkinson’s treatment be and why might side effects be seen?

A

Levodopa (dopamine precursor) can cross the BBB and is then converted to dopamine by dopa decarboxylase
Peripheral dopa decarboxylase may convert Levodopa before it crosses the BBB and then produce epinephrine which can cause arrhythmias

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59
Q

Which drug would you give with L-dopa to prevent side effects?

A

Carbidopa: dopa decarboxylase inhibitor that cannot cross the BBB

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60
Q

How would you treat Parkinson’s other than L-dopa?

A

Amantadine (antiviral that increases dopamine production)
Dopamine agonists: bromocriptine, pramipexole
Inhibitors of COMT (COMT degrades dopamine): entacapone, tolcapone
Since a loss of dopamine increases relative acetylcholine: anticholinergics- improve tremors: benzotropine

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61
Q

Give examples of other diseases in which Parkinsonism may be seen

A

Lewy body dementia
Wilson disease
Pick disease

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62
Q

Give examples of medications which may cause Parkinsonism as a side effect

A

Antipsychotics (haloperidol: blocks dopamine receptors)

Metoclopramide (dopamine antagonist, anti-emetic)

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63
Q

Describe multiple sclerosis

A

Demyelinating disease of the central nervous system

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64
Q

Which cells produce myelin in the CNS?

A

Oligodendrocytes

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65
Q

Describe the chain reaction as T cells are activated by myelin in multiple sclerosis

A

Stimulates the BBB to express more T-cell receptors and allow more immune cells to cross
T-cells release cytokines which dilate blood vessels so more immune cells can cross the BBB

Cytokines attract B cells and macrophages which produce antibodies against myelin sheath proteins, oligodendrocytes are engulfed and destroyed leaving behind areas of scar tissue

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66
Q

Give 2 genetic and 2 environmental risk factors for multiple sclerosis

A

Female, genes encoding for (HLA-DR2)

Infections, vit D deficiency

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67
Q

Describe the following patterns of MS

A

Relapsing-remitting
Secondary progressive
Primary progressive
Progressive-relapsing

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68
Q

Describe the 3 components of Charcot’s neurological triad

A

Nystagmus: plaques in nerves of eyes, involuntary rapid eye movements, loss/ blurred vision, pain/ double vision
Intention tremor: plaques along motor pathways, muscle weakness and ataxia
Dysarthria: plaques in brainstem, difficult/ unclear speech
Interfere with conscious movements, unconscious (swallowing)

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69
Q

Describe the symptoms that would result from plaques in sensory pathways in MS

A

Numbness
Pins and needles
Paresthesias

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70
Q

What is Lhermitte’s sign (in MS)?

A

Electric shock that runs down back and radiates to limbs when bending the neck forward

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71
Q

Describe the symptoms that would result from plaques in the autonomic nervous system in MS

A

Bowel/ bladder symptoms

Sexual dysfunction

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72
Q

How would you diagnose MS?

A

MRI: white matter plaques
CSF: high levels of antibodies
Visual evoked potential: measures response to visual stimuli

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73
Q

How would you treat MS?

A

RRMS:
Medications: corticosteroids, cyclophosphamide, IV Ig
Plasmapheresis: remove autoantibodies
Immunosuppressants: recombinant B-INF, decreased release of inflammatory cytokines in the brain and increased T-reg cells

Progressive MS:
Manage symptoms
Physical therapy
CBT

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74
Q

Describe the components making up CSF

A

70% lymphocytes
30% monocytes
Proteins and glucose
(Pressure 15mmHg/ 100-180mmH20)

75
Q

What is the normal total CSF volume and how much is produced each day?

A

150ml total

500ml produced/ day

76
Q

Describe meningitis

A

Inflammation of the leptomeninges (arachnoid, pia mater)

77
Q

Give 3 inflammation triggers for meningitis

A

Autoimmune disease
Adverse reaction to medication: Intrathecal therapy (injected directly into CSF
Infection: Neisseria meningitidis, Herpes simplex

78
Q

How can meningitis arise from direct spread of infection?

A

Through overlying skin
Through nose
Anatomical defect: spina bifida/ skull fracture

79
Q

How can meningitis arise from haematogenous spread of infection?

A

Binding to surface receptors
Areas of damage
Vulnerable spots e.g Choroid plexus

80
Q

What is the normal volume of WBCs in the meninges?

A

5 WBC/mm3

81
Q

Which type of meningitis has a particularly high percentage of PMNs?

A

Bacterial

82
Q

Which type of meningitis has a particularly high percentage of lymphocytes?

A

TB meningitis

83
Q

Which type of meningitis can you see the highest volume of WBCs?

A

Viral

84
Q

How do pressure, glucose conc and protein levels change in meningitis?

A

Pressure increases, glucose conc decreases, protein levels increase

85
Q

Give the common bacterial causes of meningitis in newborns, children and adults

A

Newborns: Group B strep, E.coli, Listeria
Children: Neisseria meningitidis, strep pneumoniae
Adults: strep pneumoniae, listeria monocytogenes

86
Q

Give a cause of tick-bourne meningitis

A

Borrelia Burgdoferi (cause of lyme disease)

87
Q

Give 5 viral causes of meningitis

A 
Enterovirus
Herpes simplex
HIV
Mumps
Varicella zoster
88
Q

Give 2 fungal causes of meningitis

A

Cryptococcus genuses

Coccidioids genuses

89
Q

Give a cause of parasitic meningitis

A

P. falciparum

90
Q

Give 5 symptoms of meningitis

A 
Headache
Fever
Nuchal rigidity
Photophobia
Phonophobia
91
Q

What is Kerning’s sign?

A

Lay on back, knee at 90 degrees, pain in back

92
Q

What is Brudzinski’s sign?

A

Lay on back, head lifted, knees bend

93
Q

How would you diagnose meningitis?

A

Lumbar puncture: needle between L3 and L4, takes CSF, measure pressure, analyse WBCs, protein and glucose
PCR: look for HIV, enterovirus, HSV, TB

94
Q

How would you treat meningitis?

A

Cause-dependent
Bacterial:
Steroids (to prevent injury to leptomeninges: dexamethasone)
Drugs: anti-vitals, bacterials, fungals, parasitics
Vaccine: Neisseria meningitidis, disseminated TB
Prophylactic Abx

95
Q

Give 4 causes of secondary headaches

A

Sub-arachnoid
Medication induced
Infection: meningitis
Giant cell arteritis

96
Q

Give 5 red flags accompanying headaches that may indicate a brain tumour

A

Cluster headaches
Seizures
New onset headache (associated with a Hx of cancer)
Significantly altered consciousness, memory, confusion, coordination
Papilloedema

97
Q

Describe the symptoms and pattern of a migraine

A 
4-72 hours
Unilateral, pulsing, worse with activity
Moderate to severe
Nausea and vomiting
Photophobia and phonophobia
98
Q

Which factors may worsen a migraine?

A 
Cheese
Hangover
Orgasm
Chocolate
Oral contraceptive
Lie in
Alcohol
Tumult
Exercise
99
Q

Describe the symptoms and pattern of a tension headache

A 
30mins-7 days
Mild-Moderne
Bilateral
Pressing/ tightening
Not aggravated by physical activity
Photo/ photophobia
NO nausea/ vomiting
100
Q

Describe the symptoms and pattern of a cluster headache

A 
Most severe pain
Unilateral orbital/ suborbital
15-180 minutes
Sense of restlessness/ agitation
Frequent
101
Q

How would you treat a migraine?

A

Triptan and NSAID/ paracetamol

Anti-emetic

102
Q

How can a medication overuse headache occur?

A

Underlying headache disorder
Frequent use of analgesics
Rebound headaches occur usually daily
Become chronic daily headaches

103
Q

Give 4 medications which commonly cause overuse headaches

A

Triptans
Ergotamines
Analgesics
Opioids

104
Q

Give the 2 other possible names for motor neurone disease

A

Amyotrophic lateral sclerosis

Lou Gehrig’s disease

105
Q

Describe how ALS is classified by onset

A

Limb onset: upper and lower motor neurone death, limbs affected first

Bulbar onset: motor neurons in the medulla oblongata die first with lower motor neurons
Muscles in the face, mouth and throat are affected first
Faster progression and poorer prognosis

106
Q

How would limb onset ALS present compared to bulbar onset ALS?

A

Limb: “dropped foot”, awkwardness running
Bulbar: slurred speech, dysphagia, dysphasia

107
Q

Describe the general symptoms of motor neurone disease

A

Muscle cramps, dysphagia, dysarthria, hyperreflexia, spasticity, Babinski’s sign, muscle weakness
Late stages: difficulty chewing/ swallowing: increased risk of aspiration
Decreased strength of intercostals: loss of lung function

108
Q

Give 2 possible causes/ risk factors of ALS

A

Genetics
Head injury
(90% no FHx)

109
Q

How would you manage motor neurone disease?

A 
Riluzole: protects motor neurone by reducing activity (prolongs survival)
Medications to control symptoms:
Baclofen and diazepam
Glycopyrrolate (trouble swallowing saliva)
Analgesics
Breathing support
Therapy
Nutritional advice
110
Q

Describe the differences between UMN lesions and LMN lesions

A 
UMN: Damage anywhere along corticospinal tracts
weakness affects groups
spasticity
Increased tone 
Hyperreflexia
\+ve Babinski sign

LMN: Damage anywhere from the anterior horn cells distally
Affected muscles show wasting and fasciculation
Hypotonia/ flaccidity
Reflexes are reduced/ absent

111
Q

Give 3 symptoms of autoimmune encephalitis

A

Catatonia
Psychosis
Abnormal movements

112
Q

Give 4 causes of viral encephalitis

A

Herpes simplex
Rabies
Poliovirus
Measles

113
Q

Give 3 causes of bacterial encephalitis

A

Syphilis
Meningitis
Malaria (immunocompromised)

114
Q

Give 4 symptoms of limbic encephalitis

A

Disorientation
Disinhibition
Memory loss
Seizures

115
Q

Give 4 general symptoms of encephalitis

A

Fever
Headache
Confusion
Seizures

116
Q

How would you diagnose encephalitis?

A 
MRI
EEG
Lumbar puncture
Blood test
Urinalysis
117
Q

How would you treat encephalitis?

A 
Antiviral medication
Abx
Steroids to reduce swelling
Sedatives for restlessness
Acetaminophen for fever
118
Q

How might herpes zoster virus present?

A

Chicken pox: fever, malaise headache, abode pain
Rash: pruritic, erythematous, crust (infectious 1-2 days pre and 5 days post-rash development)

Shingles: painful, hyper-aesthetic area, then macular becomes a vesicular rash
May become a disseminated infection if immunosuppressed

119
Q

How would you treat herpes zoster virus infection?

A

Oral aciclovir/ valaciclovir (within 48 hours of rash)

IV aciclovir if pregnant/ immunosuppressed

120
Q

What percentage of childhood tumours are brain tumours?

A

20%

121
Q

In general, where are brain tumours found in adults and where in children?

A

Adults: supratentorial compartment
Children: infratentorial compartment

122
Q

How might a brain tumour present?

A 
Cluster headaches
Papillary oedema
Focal deficits
Seizures: olfactory aura and deja vu
Loss of function
Drowsiness
Nausea/ vomiting
123
Q

How might brain tumours be classified according to cells affected?

A 
60% neuroepithelial: astrocytic/ oligodendritic
7% cranial/ spinal nerve tumours
28% meningeal
4% lymphomas
1% germ cell tumours
124
Q

What is the WHO grading system for brain tumours?

A

Grade 1: Pilocytic astrocytoma (benign)
Grade 2: Diffuse astrocytoma (pre-malignant: 5-7 year prognosis)
Grade 3: Anaplastic astrocytoma (2-5 year prognosis)
Grade 4: Glioblastoma, most common type (<1 year prognosis)

125
Q

Which mutations are associated with an astrocytoma and an oligodendroglioma?

A

Astrocytoma: IDH1 mutant
Oligodendroglioma: IDH1 and 1P 19Q mutant

126
Q

Describe a medulloblastoma

A

WHO grade 4 most commonly
“Small blue tumour” of the cerebellum
Common in childhood
Rapidly fatal if untreated

127
Q

Where are the common sites of brain metastases?

A 
Lung
Breast
GI
Kidney
Melanoma
128
Q

How would you treat a brain tumour?

A

Aggressive surgery if possible

Radiotherapy with adjuvant chemo (Temozolomide)

129
Q

Give 4 causes of spinal cord compression

A

Tumour
Vertebral fracture
Abscess
Ruptured intervertebral disc

130
Q

How might tumours grow within the spinal cord?

A

Causing vertebral displacement (mass effect on cord)
Tumours can grow para-spinally into the foramen
Epidural: between the disc then superiorly and inferiorly

131
Q

Describe the 4 symptom groups of spinal cord compression

A

Back pain: first symptom, progressively worse, localised pain
Motor weakness: paralysis if severe
Sensory changes: less common, clinically useful
Bladder and bowel dysfunction: urinary retention and outflow incontinence

132
Q

Give 4 common sources of mets in the spinal cord

A

Breast
Myeloma
Nasopharynx
Prostate

133
Q

How would you diagnose spinal cord compression?

A

MRI

CT with contrast (can’t see spinal oedema/ lesions well)

134
Q

How would you manage spinal cord compression?

A

Steroids to reduce inflammation e.g prednisolone

+/- surgery/ radiotherapy

135
Q

Describe and explain the symptoms of cauda equina syndrome

A

Compression of the cauda equina nerves, usually disc herniation from above
This can cause bladder/ bowel dysfunction
+ saddle/ perianal numbness
+ severe paralysis down the legs/ tingling and numbness

136
Q

How would you manage cauda equina syndrome?

A

Laminectomy

137
Q

How can you differentiate cauda equina syndrome from sciatica?

A

Sciatica doesn’t cause bladder and bowel dysfunction

138
Q

Give the 4 types of sensory fibres affected in peripheral neuropathies and the associated symptoms

A

A-alpha: loss of proprioception, sensory ataxia
A-beta: loss of light touch, pressure and vibration sensations
A-delta: myelinated- pain and cold temp (loss of)
C fibres: unmyelinated- pain and warm temp (loss of)

139
Q

Give 5 motor symptoms of peripheral neuropathy

A 
Muscle cramps
Weakness 
Fasciculations
Atrophy
High arches
140
Q

Describe the 3 clinical phenotypes of peripheral neuropathy

A

Symmetrical sensory motor: longest fibres, hands and feet, initially sensory

Asymmetrical sensory: uncommon, patchy distribution of symptoms, dorsal route ganglia affected (sensory ganglionopathy)

Asymmetrical sensory motor: mononeuritis multiplex

141
Q

How would you diagnose peripheral neuropathy?

A

Clinical exam: reduced tendon reflexes, sensory deficits, muscle atrophy/ weakness
Neurophysiological exams: nerve stimulation- how well it transmits to determine whether it’s demyelinating or axonal damage
(Demyelination: reduced conduction, axonal: reduced amplitude)

142
Q

Give 6 systemic diseases associated with axonal damage

A 
Diabetes
Vit D deficiency
Coeliac
Excess alcohol
CKD
Hypothyroidism
Connective tissue diseases
Amyloidosis
143
Q

Give 5 Inflammatory/ immune conditions associated with axonal damage

A

HIV
Hepatitis
Lyme disease
Vasculitis

144
Q

Give two immune mediated conditions associated with demyelination

A

Chronic inflammatory demyelinating PN

Multifactorial motor neuropathy

145
Q

Give a genetic cause of demyelination

A

Charcot-Marie-Tooth disease

146
Q

Describe Gullian-Barre syndrome

A

Acute neuropathy
Demyelinating/ axonal motor/ sensory motor
Rapidly ascending paralysis and sensory defects
Caused by infection elsewhere/ autoimmune

147
Q

How would you manage peripheral neuropathy?

A

Treat underlying cause/ symptoms
Balance: physio
Cramps: quinine
Pain: amitryptaline, gaba-pentin, gaba-bal

148
Q

How would you manage Gullian Barre syndrome?

A

IVIg, plasma exchange (plasmapheresis)

149
Q

Which nerve is affected in Bell’s palsy and what are the associated symptoms?

A 
Facial nerve (VII)
Symptoms:
Flattening of the forehead
Sagging of the eyebrow
Difficulty closing the eye and mouth (ipsilaterally)
Problems with feeding/ speech
150
Q

Give 6 causes of oculomotor nerve palsy (III)

A 
Autoimmune: myasthenia gravis
Complication of surgery
Vascular disorders
Tumours/ lesions
Inflammation/ infection
Trauma
Demyelinating disease (MS)
151
Q

How might the eye be affected in oculomotor nerve palsy?

A

Affected eye pupil rolls down and out (inferio-laterally)
Ptosis (drooping of eyelid)
Mydriasis (pupil dilation)
Limitations of eye movement, unable to maintain normal alignment can cause diplopia

152
Q

Describe typical trigeminal neuralgia

A

Episodes of severe, sudden, shock-like pain in one side of the fat that lasts for seconds-a few minutes
Episodes may be triggered by any touch to the face

153
Q

Give 5 causes of trigeminal neuralgia

A 
Loss of myelin around trigeminal nerve due to:
Compression from a blood vessel
MS
Stroke
Trauma
Tumour
Arteriovenous malformation
154
Q

How would you treat trigeminal neuralgia?

A

Carbamazepine (anti-convulsant)
Gabapentin (treat neuropathic pain)
Amitriptyline
Baclofen (to treat spasticity)

155
Q

Describe Brown-Sequard syndrome

A

Hemiparaplegia

Hemianaesthesia (on contralateral side)

156
Q

Describe anterior cord syndrome

A

Below injury level, motor paralysis and loss of pain/ temp

Proprioception, touch and vibration preserved

157
Q

Describe posterior cord syndrome

A

Motor function preserved

Loss of pressure, stretch and proprioception

158
Q

Describe central cord syndrome

A

Results from cervical spine injury
Greater motor loss in upper body compared to lower
Variable sensory loss

159
Q

Describe carpal tunnel syndrome

A

Compression of the median nerve causing pain, numbness and tingling, usually due to inflammation of nearby tendons and tissues

160
Q

Describe the components of the carpal tunnel

A

Bony carpal arch: posterior, floor of carpal tunnel
Flexor retinaculum: Palmar side, roof of carpal tunnel
Running through: flexor tendons for fingers and thumbs, median nerve

161
Q

Describe the symptoms of carpal tunnel syndrome

A

Initially dull ache/ discomfort
Eventually pins and needles, sharp pain/ parasthesia can extend up forearm
Muscle weakness
Thenar muscle wastage

162
Q

Why is there no loss of central palmar sensation in carpal tunnel syndrome?

A

Palmar branch is unaffected

163
Q

Give 3 risk factors for carpal tunnel syndrome

A

Obesity
Pregnancy
Underlying conditions (rheumatoid arthritis)

164
Q

How would you diagnose carpal tunnel syndrome?

A

Electrophysiological testing
Description of symptoms
Physical tests

165
Q

What is Tinel’s sign for carpal tunnel syndrome?

A

Tapping median nerve, symptoms of tingling/ pins and needles

166
Q

What is Phalen’s manoeuvre for carpal tunnel syndrome?

A

Flex wrists for 1 min, numbness in innervated areas

167
Q

What is Durkan’s test for carpal tunnel syndrome?

A

Manually compress transverse carpal ligament for 30s

Symptoms arise

168
Q

How would you treat carpal tunnel syndrome?

A 
Behaviour modification
Physical therapy
Splinting
Corticosteroids
Surgical division of the transverse carpal ligament
169
Q

Describe myasthenia gravis

A

Autoimmune disease affecting skeletal muscle, patients often wake up feeling fine but weak by the end of the day

170
Q

Which groups are preferentially affected by myasthenia gravis?

A

Young women 20-30s

Older men 60s-70s

171
Q

Describe the pathology of myasthenia gravis

A

B-cells produce antibodies which bind to nicotinic acetylcholine receptor on muscle cell membrane, preventing acetylcholine binding

Antibodies also activate the classical compliment pathway causing inflammation and muscle cell destruction

B-cells also produce muscle specific receptor tyrosine kinase antibodies which target proteins in muscle cells

172
Q

How can myasthenia gravis present as paraneoplastic syndrome?

A

Underlying cancer
Bronchogenic carcinoma/ thyme neoplasm
Causes a B-cell autoimmune response

173
Q

What is a myasthenic crisis?

A

Decrease in function of muscles controlling breathing

174
Q

How would you treat myasthenia gravis?

A 
Acetylcholinesterase inhibitors (neostigmine/ pyridostigmine): stops Ach breakdown
Immunosuppressive drugs: prednisone (reduce production of autoantibodies
Surgical removal of the thymus: reduces muscle weakness
175
Q

Describe the mutation that causes Huntington’s disease

A

Autosomal dominant

Huntingtin (HTT): chromosome 4 contains a triplet repeat

176
Q

How many repeat and of which sequence would usually cause Huntington’s?

A

> 36 CAG repeats (which codes for amino acid glutamine)

177
Q

How does the mutated Huntingtin protein cause symptoms of Huntington’s?

A

Mutated protein builds up in the putamen and caudate of the basal ganglia, causing cell death (excitotoxicity) this causes excessive signalling and an increase in intracellular Ca2+

178
Q

Describe what is meant by anticipation in the context of Huntington’s

A

Due to divisions, child can inherit more CAG repeats than the parents had
More repeats often means earlier onset

179
Q

How does the parent affected change the likelihood of anticipation in Huntington’s?

A

Repeated expansion happens more with sperm production than egg
Anticipation and new disease alleles are more likely to happen if the father is affected

180
Q

Describe the symptoms of Huntington’s disease

A 
Movement problems:
Chorea: dance-like/ jerking movements
Athetosis: slow movements
Abnormal eye movements
Poor co-ordination

Psychological problems:
Dementia
Personality changes
Depression

181
Q

What is the result of dorsal striatum neuronal death in Huntington’s?

A

Loss of brain tissue and expansion of lateral ventricles

182
Q

What is the typical age of onset of Huntington’s?

A

40 y/o

183
Q

What is the effect on neurotransmitter levels in Huntington’s?

A

Loss of GABA
Loss of acetylcholine
Increased levels of dopamine

184
Q

How might you treat chorea as a symptom of Huntington’s?

A

Neuroleptics: dopamine receptor antagonists
Tetrabenazine: depletes dopamine

Medicine Phase 2A (OWN) (10 decks)

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