Brainscape's Knowledge GenomeTM

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


See full index

Phase 2a Sheffield Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

What is an upper motor neurone?

A

A neurone located entirely in the CNS. The cell body is located in the primary motor cortex.

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

What are the signs of UMN weakness?

A
  1. Spasticity
  2. Increased muscle tone
  3. Hyper-reflexia
  4. Minimal muscle atrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the causes of UMN weakness?

A
  1. MS
  2. Brain tumour
  3. Stroke
    Heredity spastic paraplegia affects UMN’s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the signs of spastic paraplegia?

A
  1. Abnormal gait
  2. Bladder problems
  3. High arched feet
  4. Increased tone in legs and minimal muscle wasting
  5. Family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How many people with alzheimer’s develop Parkinsonism?

A

25%

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

What are the symptoms of Alzheimers

A
  1. Selective attention
  2. Language impairments – difficulty in naming and understanding
  3. Apraxia
  4. Global deficits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the first cognitive marker of Alzheimer’s?

A

First cognitive marker is usually short term memory impairment

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

What are the histological signs of Alzheimers?

A
  1. Plaques of amyloid

2. Neuronal reduction

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

How is Alzheimer’s disease diagnosed?

A

When criteria (Braak Staging) for intermediate or high likelihood of AD is met and history of dementia

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

What is the stages in Braak staging?

A
  1. Stage ½ - low likelihood
  2. Stage ¾ - intermediate likelihood
  3. Stage 5/6 – low likelihood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the cause of sematic dementia?

A

symmetrical temporal lobe atrophy

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

What is functional memory dysfunction?

A

acquired dysfunction of memory that significantly affects a persons private/professional life in the absence of organic abuse.

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

How can you determine whether it is function memory or degenerative disease?

A
  1. Ask when was the last time your memory let you down
  2. Someone with dysfunction – good detailed answer
  3. Someone with degenerative – would struggle to answer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is brain function assessed?

A

fMRI and PET scans

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

What is the treatment for Alzheimer’s?

A
  • Ace inhibitors e.g. galantamine

- Supportive care

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

What is dementia?

A

A set of symptoms that include memory loss and difficulties when thinking, problem solving or language. A disease with a progressive decline in cognitive function

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

What is the epidemiology of dementia?

A

10% over 65 have dementia and 20% over 80 have it.

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

What are the causes of dementia?

A
  1. Alzheimers disease (65%)
  2. Fronto-temporal disease – frontal lobe atrophy on MRI
  3. Vascular
  4. Lewy body
  5. Vitamin deficiency e.g. B12
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the symptoms of fronto-temporal dementia symptoms?

A
  1. Behaviour variants
  2. Language variants
  3. Often overlaps with MND
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What other disease is dementia closely associated to?

A

MND

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

What is the function of the temporal lobe?

A

hearing, language comprehension, memory and emotion

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

What other disease affects the temporal lobe?

A

Alzheimer’s

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

What investigations would you pursue in suspected dementia?

A
  1. Good history of Symptoms
  2. 6CIT – 6 cognitive impairment items
  3. Blood tests –> b12 deficiency
  4. MRI
  5. Amyloid and tau histopathology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do you prevent dementia?

A
  1. Stop smoking
  2. Healthy diet
  3. Regular exercise
  4. Healthy weight
  5. Low alcohol intake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the treatment for dementia?

A

Occupational therapy

Acetylcholine Esterase inhibitors

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

What is Spondylolisthesis?

A

Spillage of vertebra over the one below

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

What is Spondylosis?

A

degenerative disc disease

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

What is Myelopathy?

A

Spinal cord disease, UMN problem

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

What is radiculopathy?

A

Spinal nerve root disease, LMN problem

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

What is weakness?

A

impaired ability to move a body part in response to will

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

What is paralysis?

A

Ability to move a body part in response to will is completely lost.

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

What is ataxia?

A

willed movements are clumsy and uncontrolled

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

What is involuntary movements?

A

Spontaneous movement independent of will.

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

What is apraxia?

A

The ability to carry out familiar purposeful movements is lost in the absence of paralysis or other sensory/motor impairments

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

What type of inheritance has huntington’s disease got?

A

AD inheritance

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

What does huntingtons disease affect?

A

The striatum (caudate nucleus) of the basal ganglia.

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

What Neurotransmitter does HD affect?

A

GABA

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

What are the early signs of HD?

A

Irritability, depression and personality change

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

What are the late signs of HD?

A

chorea, psychiatric problems and dementia

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

How is dopamine produced?

A

Tyrosine –> l-dopa –> dopamine

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

What is the pathophysiology of PD?

A
  • Loss of dopamine producing hormones in the substantia nigra
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What does the substantia nigra project too?

A

Striatum.

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

What are the symptoms of PD?

A
  1. Bradykinesia – problems; doing up buttons, shuffle walking, writing smaller etc
  2. Rigidity – pain, problems turning in bed
  3. Resting tremor
  4. Postural instability
  5. Depression, psychiatric problems, dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Is the presentation of parkinson’s disease symmetrical?

A

No. It is asymmetrical with one side being worse than the other.

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

What is the treatment of Parkinson’s disease?

A
  1. L dopa
  2. Dopamine agonists – ropinirole, cabergoline
  3. COMT/MAO inhibitors – selegiline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the histopathological signs of Parkinsons disease?

A

Lewy bodies

Loss of dopaminergic neurones in the substantia nigra

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

What area of the brain does deep brain stimulation affect?

A

sub-thalamic nucleus

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

What is the treatment for essential tremor?

A

beta blockers, primidone

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

What are the 4 main stages of PD?

A
  1. Resting tremor
  2. Bradykinesia
  3. Postural istability
  4. Rigidty
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the symptoms of trigeminal neuralgia?

A
  1. Unilateral face pain
  2. Pain commonly in V3 distribution
  3. Electric shock like shooting/sharp pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How long does trigeminal neuralgia last?

A

a few seconds

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

What are the activities that make trigeminal neuralgia worse?

A

Washing your face, eating, shaving and talking

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

What is encephalitis?

A

Inflammation of the brain.

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

What are the symptoms of encephalitis?

A
  1. Fever
  2. Headache
  3. Lethargy
  4. Behavioural change
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What would a lumbar puncture show in a patient with encephalitis?

A
  1. Lymphocytosis
  2. Raised protein
  3. Normal glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What viruses can cause encephalitis?

A
  1. Herpes simplex
  2. Varicella zoster
  3. HIV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the treatment for encephalitis?

A

Acyclovir

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

Who is encephalitis more common in?

A

The immunocompromised.

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

If a patient has aphasia which area is affected?

A

Broca’s area

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

If a patient has receptive dysphasia which area is affected?

A

Wernicke’s area

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

What are muscle spindles innervated by?

A

Gamma motor neurones

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

What is the function of muscle spindles?

A

Control muscle tone and tell you how much a muscle is stretched

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

What is the cause of pyramidal pattern of weakness in the upper limb?

A

The flexors are stronger than the extensors.

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

What is the cause of pyramidal pattern of weakness in the lower limb?

A

The extensors are stronger than the flexors.

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

What is the treatment for sciatica without neurological signs?

A

Conservative management and NSAIDs

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

What are the 4 signs of intra-cranial pressure rising?

A
  1. Papilloedema
  2. Focal neurological signs
  3. Loss of consciousness
  4. New onset seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the signs of normal pressure hydrocephalus?

A
  1. Magnetic gait
  2. Incontinence
  3. Dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is used in the thrombolytic treatment of ischaemic stroke?

A

Altepase is used in ischaemic stroke –> converts plasminogen into plasmin so promotes breakdown of the clot.

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

How long can you do the thrombolysis on a stroke patient for after the onset of symptoms?

A

4.5 hours.

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

What condition presents with polyneuropathy?

A

GB syndrome.

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

What is the treatment for raised ICP?

A

Osmotic diuresis with mannitol

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

What is the most common cause of spinal cord compression?

A

Secondary malignancy from lung, breast, prostate and or kidney.

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

What are the symptoms of Rabies?

A
  1. Fever
  2. Anxiety
  3. Confusion
  4. Hydrophobia
  5. Hyperactivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is the cause of tetanus?

A

Clostridium tetani (gram pos anaerobe) causes tetanus

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

What are the symptoms of tetanus?

A
  1. Trismus (lockjaw)
  2. Sustained muscle contraction
  3. Facial muscle involvement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the cause of botulism?

A

Clostridium botulinum

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

What are the symptoms of botulism?

A
  1. Diplopia (Double vision)
  2. Dysphagia
  3. Peripheral weakness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What 3 Organisms can cause meningitis?

A
  1. N. meningitidis (G-ve diplococci)
  2. S. pneumoniae (g+ve cocci chain)
  3. Listeria monocytogenes (g+ve bacilli) –> shows as gram positive film
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are 3 organisms that can cause meningitis in children?

A
  1. E.coli (G-ve bacilli)
  2. Group B streptococci e.g. s.agalactiae
  3. Listeria monocytogenes –> shows as gram positive film
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

How would a listeria infection causing meningitis be treat?

A

Cefotaxime and amoxicillin

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

What are the symptoms of meningitis?

A
  1. Non blanching petechial rash
  2. Neck stiffness
  3. Headache
  4. Photophobia
  5. Papilloedema
  6. Fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What investigations would you order if you suspected meningitis?

A
  1. Blood cultures
  2. Bloods – FBC, U+E, CRP, Serum glucose, lactate
  3. Lumbar puncture
  4. CT head
  5. Throat swabs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the management for meningitis?

A
  1. Treat with antibiotics –> Cefotaxime
  2. Cefotaxime + amoxicillin if L.monocytogenes infection
  3. Steroids to reduce inflammation in S.pneumoniae infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the meningitis vaccine schedule?

A
  • Meninigits B - 8-16 Weeks
  • Meningitis C - 12 weeks and 1 year
  • Meningitis ACWY - 14 years old
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What prophylaxis is effective against N. meningitidis?

A

Ciprofloxacin

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

What is the most common cause of viral meningitis?

A

Enterovirus

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

What is the CSF like in bacterial meningitis?

A

Cloudy

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

What is the CSF like in someone with viral meningitis?

A

High lymphocytes, normal/high protein + normal glucose

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

What is the CSF like in someone with bacterial meningitis?

A

High neutrophils, protein and low glucose

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

What are the potential side affects of a lumbar puncture?

A
  1. Headache
  2. Damage to spinal cord
  3. Paraesthesia
  4. CSF leak
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What investigations could you do on a CSF sample?

A
  • Protein and glucose levels
  • MCS
  • Bacterial and Viral PCR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is a LMN?

A

A neurone that carries signals to effectors. The cell body is in the brain stem or spinal cord.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What are the signs of LMN weakness?

A
  1. Flaccid
  2. Reduced muscle tone
  3. Hypo-reflexia
  4. Muscle atrophy
  5. Fasciculations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Where are the cell bodies of LMN found?

A

LMN cell bodies are found in the spinal cord or in the cranial nerve nuclei in the brainstem.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What investigations would you do if you suspected LMN issues?

A
  1. EMG
  2. MRI
  3. Muscle enzyme
  4. Lumbar puncture –> CSF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What diseases are associated with motor neuron damage?

A
  1. MN disease
  2. Spinal atrophy
  3. Poliomyelitis
  4. Spinal cord compression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What are 5 sites of damage along the final common pathway?

A
  1. Cranial nerve nuclei
  2. MN
  3. Spinal ventral roots
  4. Peripheral nerves
  5. NMJ –> cause of Myasthenia Gravis
  6. Muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What pathologies are associated with ventral spinal root damage?

A
  1. Tumours
  2. Prolapsed intervertebral disc
  3. Cervical/lumbar spondylosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What are the signs of UMN damage?

A
  1. Motor cortex lesions
  2. Internal capsule
  3. Brainstem
  4. Spinal cord
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What are the clinical patterns associated with Motor Neurone disease?

A

Muscular atrophy – anterior horn lesion –> LMN, fasciculations, weakness and wasting

Amytotrophic lateral sclerosis – loss of neurones in MC and anterior horn of the SC –> LMN and UMN signs –>
progressive spastic tetra-paresis

Progressive bulbar palsy –> destruction of Cn 9-12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What might someone with progressive bulbar palsy present with?

A
  • Dysphagia
  • Dysarthia (slurred speech)
  • Wasting and fasciculations of the tongue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What is a long term consequence of ALS?

A

Progressive spastic tetraparesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What are the onset limb symptoms of MND?

A
  • Weakness/clumsiness
  • Wasting of muscles
  • Foot drop and tripping
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What are the onset bulbar symptoms of MND?

A
  1. Dysarthria
  2. Slurred speech
  3. Dysphagia
  4. Wasting and fasciculation of tongue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What are the respiratory symptoms of MND?

A
  1. Dyspnoea
  2. Orthopnoea
  3. Poor sleep
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What is treatment for MND?

A

Riluzole – inhibits glutamate release and slows disease progression

Ventilatory support

Feeding by a PEG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What is a TIA?

A

An acute loss of cerebral or ocular function with symptoms lasting <24hrs and with a complete clinical recovery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What are the causes of a TIA?

A

Inadequate cerebral blood flow –> ischaemia or embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What is the use of the ABCD2 score?

A

Essential to assess their risk of having a stroke in the next 7 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What is the ABCD2 score?

A
  • Age >60
  • BP –> 140/90
  • Clinical features –> unilateral weakness/speech disturbance
  • Duration
  • Diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What is the management of a TIA?

A

Control BP –> statins and aspirin/clopidogrel

112
Q

What is Guillain-Barre’s syndrome?

A

Acute neuropathy caused by Autoimmunity when healthy nerve cells are destroyed in the PNS.

113
Q

What is the cause of Guillain-barre’s syndrome?

A

Often post op infection following CMV, EBV and after a campylobacter jejuni infection

114
Q

What are the symptoms of Guillain-barre’s syndrome?

A
  1. Ascending muscle weakness

2. Changes in sensation and pain

115
Q

What can non-missle trauma to the scalp cause?

A

Contusion and laceration

116
Q

What can non-missle trauma to the skull cause?

A

Skull fracture

117
Q

What can non-missle trauma to the brain cause?

A

Contusions, lacerations, hemorrhages and infection

118
Q

What can diffuse vascular trauma to non missile trauma cause?

A

Multiple potential hemorrhages.

119
Q

What are 2 risks associated with skull fracture?

A
  1. Haematoma

2. Infection

120
Q

What is the aetiology of diffuse traumatic axonal injury?

A
  • Acceleration/deceleration –> shearing rotational forces –> axonal tearing
121
Q

What is the mechanism behind acceleration/deceleration?

A
  • Force to head causes differential brain movements -> shearing and compressive stress
  • This increases the risk of axon tear and blood vessel damage.
122
Q

What is a contusion?

A

Superficial brain bruse

123
Q

What is a laceration?

A

When a contusion is sever enough to tear the pia mater.

124
Q

What are 3 examples of primary headaches?

A
  • Migraine
  • Tension headaches
  • Cluster headaches.
125
Q

What is the most common secondary headache?

A

medication overuse headache

126
Q

What are 3 examples of secondary headaches?

A
  • Meningitis
  • Subarachnoid haemorrhage
  • Giant cell arteritis
  • Medication overuse headaches
127
Q

What are 5 important questions to ask when a patient presents with headaches?

A
  1. Time – Onset, duration, frequency and pattern
  2. Pain – Severity, quality, site and spread.
  3. Associated symptoms e.g. nausea, vomiting, photophobia, phonophobia
  4. Triggers/aggravating/relieving factors
  5. Response to attack – does medication work?
  6. What are the symptoms between attacks?
128
Q

What are 5 red flags for suspected brain tumour?

A
  1. New onset headache and history of cancer
  2. Cluster headache
  3. Seizure
  4. Significantly altered consciousness, memory or confusion
  5. Other abnormal neuro exams
  6. Papilloedema (swollen optic disc)
129
Q

How long do migraines last?

A

4-72 hours

130
Q

What is migraine pain like?

A
  1. Unilateral
  2. Throbbing
  3. Moderate to severe pain
  4. Aggravated by physical activity

May also experience photophobia and or phonophobia. As well as nausea but no vomiting.

131
Q

What can headaches be subdivided into?

A
  • Episodic 20% with aura and 80% without

- Chronic migraine

132
Q

What might a patient with an aura complain of?

A
  1. Visual disturbances e.g. flashing lights
  2. Sensory disturbances e.g. tingling in hands and feet
  3. Language aura and motor aura
133
Q

What is the treatment for migraines?

A
  1. Ensure accurate diagnosis
  2. Lifestyle modification and trigger management
  3. Psychological and behaviour treatment
  4. Abortive treatment; PO triptan and NSAIDs
  5. Anti-emetics
  6. Preventive treatment –> propranolol, acupuncture and amitriptyline
134
Q

What is the most common type of primary headache?

A

tension headache

135
Q

How long do tensions headaches last?

A

30 mins to 7 days

136
Q

How can you diagnose a migraine without an aura?

A
  • 5 attacks lasting between 4-72 hrs w/ nausea /vomiting or photo/phonophobia
  • Unlateral throbbing pain
  • Pain aggravated by physical activity
137
Q

What are the triggers of migraines?

A

Cheese, OCP, Alcohol, caffeine, anxiety, travel and exercise

138
Q

What is the pain associated with tension headaches?

A
  1. Bilateral
  2. Pressing/tight
  3. Mild/moderate pain
  4. Not aggravated by physical activity

Wouldn’t have any other symptoms.

139
Q

What is the criteria for diagnosing medication overuse headaches?

A
  1. Headache present for 1 in every 2 days
  2. Regular use for more than 3 months and symptomatic for over 1
  3. Headache has developed or worsened during drug use.
140
Q

What is the pain of a cluster headache?

A
  1. Severe/very severe pain
  2. Pain around the eye/temporal area
  3. Unilateral
  4. Headache is accompanied by cranial autonomic features.
141
Q

How long do cluster headaches last for?

A

15 mins to 3 hrs

142
Q

What 4 features of a headache might make you suspect meningitis?

A
  1. Non blanching – purpura rash
  2. Neck stiffness
  3. Photophobia
  4. Pyrexia
143
Q

What investigations could you do with headaches when the cause is unknown?

A
  1. Bloods
  2. Blood cultures
  3. Throat swab
  4. Blood for serology and PCR
  5. CT Head
144
Q

What nerve does carpal tunnel syndrome affect?

A

Median nerve

145
Q

What are the risk factors of carpal tunnel syndrome?

A
  • Prengnacy
  • Obesity
  • RA
  • Hypothyroidism
  • Acromegaly
146
Q

What investigations would you do in carpal tunnel syndrome?

A

Tinnel’s and Phalen’s test

147
Q

What is MS?

A

A chronic auto-immune disorder of the CNS characterised by an inflammatory and demyelinating disease characterised by progressive disability.

148
Q

Describe the pattern of MS?

A
  • Patients will have multiple attacks over the years, there is no progression between attacks
  • It is a slow and progressive disease, leading to a slow decline in neurological functions
  • Can be exacerbated by Heat –> warm shower
149
Q

What is the epidemiology of MS?

A
  • Presents between 20-40, affects more females and rarer in tropics.
150
Q

What is the aetiology of MS?

A
  • Environment – e.g. EBV infection is associated
  • Genetic predisposition
  • Chance
151
Q

What is the pathophysiology of MS?

A
  1. Genetic susceptibility + environmental trigger –> T cell activation
  2. B cell and macrophage activation –> inflammation, demylination and axon destruction

Myelin eventually regenerates but thinly so it’s less efficient.

152
Q

What are the major features of MS plaque?

A
  1. Inflammation
  2. Demyelination
  3. Axon loss
  4. MS plaques are seen histologically around the blood vessels – perivenular.
153
Q

What are the signs of MS?

A
  1. Spasticity
  2. Nystagmus + double vision
  3. Optic neuritis - impaired vision and pain
  4. Sensory symptoms
  5. Weakness
  6. Bladder + sexual dysfunction
  7. Paresthesia
154
Q

What are atypical symptoms of MS?

A

if a patient has them they are unlikely to have MS

  1. Aphasia
  2. Hemianopia
  3. Muscle wasting
155
Q

What is the diagnostic criteria for MS?

A
  1. > 2 CNS Lesions dessimated in time and space

2. Exclusion of conditions that may give a similar clinical presentation

156
Q

What are 3 differential diagnoses of MS?

A
  1. SLE
  2. Sjogren’s
  3. AIDs
157
Q

What investigations would you order in suspected MS?

A
  1. MRI or brain and spinal cord – lesions may be seen around ventricles
  2. Lumbar puncture – CSF

Electrophoresis of CSF would show oligoclonal IgG bands

158
Q

What is the management of MS?

A
  • Short course steroids to reduce severity  methylprednisolone
  • Beta-interferons (anti-inflammatories)
  • Stem cell transplants
  • Muscle relaxants for spasticity
  • Natalizumab
159
Q

What is the non pharmacological management of MS?

A
  1. Psychological therapies and counselling
  2. Speech therapists
  3. Physiotherapy and occupational therapy.
160
Q

What is myasthenia gravis?

A

Myasthenia gravis is an AI disorder. AI antibodies (IgG) attach to Ach receptors. It causes abnormal weakness.

161
Q

What are the symptoms of myasthenia gravis?

A

Weakness and fatigue

162
Q

What investigations would you order in myasthenia gravis?

A
  1. Serum anti-Ach receptor antibodies

2. Ask the patient to count to 50

163
Q

What autoantibodies would be present in myasthenia gravis?

A
  1. Anti-AchR antibodies

2. Antibodies against tyrosine kinase

164
Q

A patient complains of having a seizure. An eye-witness account tells you that the patient had their eyes closed, was speaking and there was waxing/waning/pelvic thrusting. They say the seizure lasted for about 5 minutes. Is this likely to be an epileptic or a non-epileptic seizure?

A

Likely to be non-epileptic

165
Q

A patient complains of having a seizure. An eye-witness account tells you that the patient was moving their head and biting their tongue. They say the seizure lasted for just under a minute. Is this likely to be an epileptic or a non-epileptic seizure?

A

Likely to be epileptic

166
Q

A patient complains of having a ‘black out’. They tell you that before the ‘black out’ they felt nauseous and were sweating. They tell you that their friends all said they looked very pale. Is this likely to be due to a problem with blood circulation or a disturbance of brain function?

A

likely due to a blood circulation problem e.g. syncope.

167
Q

You see a patient who you suspect has meningitis. It is noted that they have raised ICP. Would you do a lumbar puncture?

A

NO! You would not do a lumbar puncture due to the risk of coning.

168
Q

What muscle is essential for correcting the extorsion action of lateral rectus when walking downstairs

A

Superior oblique CN4 innervations

169
Q

What muscle needs to be in working around to test the action of the superior and inferior rectus

A

Lateral rectus –> patient is first asked to abduct their eyes 30 degrees, requiring the LR.

170
Q

How can the Superior and inferior oblique can be tested

A

Position the eye so the superior and inferior recti are giving maximum rotation and giving complete correction.

171
Q

What is the function of the cerebellum?

A

Precise control, fine adjustment and coordination of motor activity based on continual sensory feedback.

It controls how you do something –> adjusts for error

172
Q

What are the layers of the cerebellum?

A
  1. Molecular
  2. Purkinje layer
  3. Granular layer
173
Q

What are 5 signs of cerebellar dysfunction?

A
  1. Dysdiadochokinesia – inability to perform rapid, altering movement
  2. Ataxia
  3. Nystagmus
  4. Intention tremor
  5. Slurred speech
  6. Hypotonia
174
Q

How can you classify ataxia severity?

A
  • Mild – independent or 1 walking aid
  • Moderate – patient requires 2 walking aids
  • Severe – patient is wheelchair dependent
175
Q

What is friedrichs ataxia?

A

An AR inherited cerebellar ataxia which presents in early childhood and increases the risk of diabetes/CV problems.

176
Q

What is spinocerebellar ataxia?

A

AD inherited cerebellar ataxia which presents with difficulty focusing and migraines

177
Q

What are the causes of acquired cerebellar ataxia?

A
  1. Toxic e.g. alcohol and lithium
  2. Idiopathic
  3. Neurodegenerative
  4. Immune mediated
178
Q

What is an example of immune mediated cerebellar ataxia?

A
  1. Post infection cerebllitis
  2. Gluten ataxia
  3. Para-neoplastic cerebellar degeneration (secondary from lung or breast)
  4. Primary AI cerebellar ataxia.
179
Q

What is the cause of chronic traumatic encephalopathy?

A

often seen following repetitive mild traumatic brain injury

180
Q

What are the initial symptoms of chronic traumatic encephalopathy?

A
  1. Irritable
  2. Impulsive
  3. Aggressive
  4. Depressed
181
Q

What are the later symptoms of chronic traumatic encephalopathy?

A
  1. Dementia
  2. Gait and speech problems
  3. PD symptoms
182
Q

What are the signs of chronic traumatic encephalopathy?

A
  1. Atrophy of Deep brain structures
  2. Enlarged ventricles
  3. Tau deposited in sulci
183
Q

What is the epidemiology of giant cell arteritis?

A
  • Affects those >50y/o
  • Incidence increases with age
  • Twice as common in women
184
Q

What are the symptoms of giant cell arteritis?

A
  • Headache
  • Scalp tenderness
  • Jaw claudication
  • Acute blindness
  • Malaise
185
Q

What is giant cell artertis?

A

Temporal arthritis –> inflammation of the large blood vessels in head neck and arms.

186
Q

What are the investigations in giant cell arteritis?

A
  1. Bloods for inflammatory markers e.g. CRP, ESR

2. Temporal artery biopsy

187
Q

What are the clinical investigation findings in giant cell arteritis?

A
  • Palpable and tender temporal arteries w reduced pulsation

- Sudden monocular visual loss, optic disc is swollen

188
Q

What are the diagnostic criteria of giant cell artertis?

A
  • Age >50
  • New headache
  • Temporal artery tenderness
  • Abnormal artery biopsy
189
Q

What is the treatment for giant cell arteritis?

A
  • Prompt corticosteroids e.g. prednisolone
  • Methotrexate sometimes
  • Osteoporosis prophylaxis is important –> lifestyle advice and vit D
190
Q

What are the 3 cardinal presenting times of a brain tumour?

A
  1. Raised ICP
  2. Progressive neurological deficit
  3. Epilepsy
191
Q

What are the signs of raised ICP?

A
  1. Headache
  2. Drowsiness
  3. Vomiting
    Cardinal sign of raised ICP is Papilloedema due to obstruction of venous return from the retina.
192
Q

Where do primary tumours originate from?

A

The glial cells

  1. Astrocytoma (90%)
  2. Oligodendroglioma (5%) – associated with defects in chromosomes 1 and 19
193
Q

What are 2 factors that worsen a brain tumour?

A
  1. Worst first thing in the morning

2. Worst when coughing, straining or bending forwards

194
Q

Where might secondary brain tumours originate from?

A
  1. Lung (NSCC)
  2. Breast
  3. Malignant melanoma
  4. Kidney
  5. Gut
195
Q

What is the treatment for secondary brain tumours?

A
  1. Surgery and adjuvant therapy
  2. Chemotherapy
  3. Supportive care
196
Q

Describe an oligodendroglioma

A
  1. All IDH1 mutation positive
  2. Chemo sensitive
  3. 10-15 year survival
197
Q

Describe the WHO glioma grading.

A
  1. Benign paediatric tumour
  2. Pre malignant tumour – Seizures and seen in young adults
  3. Anaplastic astrocytoma – cancer
  4. Glioblastoma multiforme (GBM)
198
Q

What causes grade 2 deterioration?

A
  1. Tumour transformation to malignant phenotype
  2. Progressive mass effect due to slow growth
  3. Progressive neurological deficit from functional brain destruction.
199
Q

What is the physiology of muscle contraction?

A
  1. Ca2+ released from sarcoplasmic reticulum –> T tubules
  2. Binds to troponin C which moves tropomyosin to expose a myosin binding site
  3. Myosin binds to specific areas on actin using ATP
  4. Cross bridge formation and detachment cycle
200
Q

What is dystrophin and what disease is it affected in?

A

Dystrophin – links the ECM to the cytoskeleton of a muscle fibre

  • Affected in Duchenne muscular dystrophy (X linked recessive disease)
201
Q

When does DMD present?

A

Often presents at <5 y/o, patient often in a wheelchair by 13

202
Q

What cardiac problems are associated with DMD?

A

arrhythmias, conduction block and cardiomyopathy

203
Q

What is the histology of DMD?

A

Muscle cell nuclei all over the place –> muscle cells all different shapes and sizes

Absence of dystrophin

204
Q

What is the pathophysiology of DMD?

A

Large deletions, duplications and mutations disrupt the reading frame –> out of frame mutations –> dystrophin not produced –> DMD phenotype

205
Q

What is the treatment of DMD?

A
  • Supportive – physio, OT, home adaptations
  • Scoliosis corrective surgery
  • Manage cardiac problems
  • Steroids
  • Gene therapy
206
Q

What is the inheritance in myotonic muscular dystrophy?

207
Q

What is the pathophysiology of Myotonic muscular dystrophy?

A

CTG expansion non-coding region of DMPK –> Down stream effects –> mis-splicing of proteins –> Cl- channel gene affected –> myotonia.

208
Q

What are the adult onset symptoms of myotonic muscular dystrophy?

A
  1. Myotonia – delayed relaxation after contraction
  2. Distal muscle weakness
  3. Cataracts
  4. Male hypogonadism
  5. Frontal baldness
  6. Diabetes
  7. Cardiac problems
209
Q

What is the treatment of myotonic mucsular dystrophy?

A
  • Supportive care
  • Treat cardiac issues
  • Anti-convulsants for myotonia
210
Q

What is a recessive type of msucular dystrophy?

A

Beckers muscular dystrophy - a mild type of DMD

211
Q

What is the pathophysiology of beckers MD?

A

In frame mutations so dystrophin is produced but shortened or defective.

212
Q

What is the common pathway to cause GBM?

A

Initial genetic error of glucose glycolysis –> IDH 1 mutation –> excessive build up of 2-hydroxyglutarate –> genetic instability in glial cells triggered.

213
Q

What are good prognostic factors for GBM?

A
  1. <45 yo
  2. Aggressive surgical therapy
  3. Good post op performance
  4. Secondary GBM
  5. MGMT mutant –> will respond well to chemo
214
Q

What is the treatment for GBM?

A
  1. Resective surgery

2. Adjuvant chemo with temozolomide

215
Q

What is cauda equina syndrome?

A

Spinal compression at or distal to the L1 nerve root that disrupts sensation and movement.

216
Q

What are the signs of cauda equina syndrome?

A
  1. Saddle anaesthesia
  2. ED
  3. Bladder/bowel dysfunction
  4. Variable leg weakness
  5. Bilateral sciatica –> all the way from leg to foot
217
Q

What are the investigations in cauda equina syndrome?

A

MRI of the spine

218
Q

What is a syncope?

A

Insufficient blood or oxygen supply to the brain that causes paroxysmal changes in behaviour, sensation and cognitive processes.

219
Q

What are 5 signs that transient loss of consciousness is down to syncope?

A
  1. Situational
  2. 5-30 seconds
  3. Sweating
  4. Nausea
  5. Pallor
  6. Dehydration
220
Q

What is a non epileptic seizure?

A

mental processes associated with psychological distress causing paroxysmal changes in behaviour, sensation and cognitive processes.

221
Q

What are the 5 signs of non-eplileptic seizures?

A
  1. Situational
  2. 1-20 mins –> longer than epileptic
  3. Eyes closed
  4. Crying or speaking
  5. Pelvic thrusting
  6. History of psychiatric illness
    A non-epileptic seizure will last longer than an epileptic one.
222
Q

What are the categories of epileptic seizures?

A
  1. Focal epilepsy – only one portion of brain is involved

2. Generalised epilepsy – whole brain is affected

223
Q

Give an example of focal epileptic seizures?

A

Treat with carbamazepine

  • Simple partial seizures with consciousness
  • Complex partial seizures without consciousness
  • Secondary generalised seizures
224
Q

Give an example of a generalised seizure

A

Treat with sodium valproate

  1. Absence seizures
  2. Myoclonic seizures
  3. Generalised tonic clonic seizures
225
Q

What is a generalised tonic seizure?

A

sudden onset rigid tonic phase followed by convulsion (clonic), lasts up to 120 seconds and associated with tongue biting and incontinence

226
Q

What is an absence seizure?

A

commonly present in childhood and child ceases activity and stares for a few seconds

227
Q

What are myoclonic seizures?

A

isolated muscle jerking

228
Q

What are the side effects of anti-epileptic drugs?

A
  1. Cognitive disturbances
  2. Heart disease
  3. Drug interactions
  4. Teratogenic
229
Q

What is the treatment of generalised epileptic seizures?

A

Treatment for generalised epileptic seizures –> Sodium valproate

  • Sodium valproate is teratogenic
230
Q

What is the treatment for focal epileptic seizures?

A

Treatment for focal epileptic seizures –> Carbamazepine

Carbamazepine inhibits presynaptic Na+ channels so prevents axonal firing

231
Q

What is a stroke?

A

Rapid onset of neurological deficit which is the result of a vasc lesion and is associated with infarction of CN tissue

232
Q

What is the cause of a stroke?

A
  1. Cerebral infarct due to embolism or thrombosis

2. Intracerebral or subarachnoid haemorrhage (15%)

233
Q

What is the risk factors of a stroke?

A
  1. Hypertension
  2. DM
  3. Cigarette smoking
  4. Hyperlipidaemia
  5. Obesity
  6. Alcohol
234
Q

What investigation can you do for a stroke?

A

can determine whether its haemorrhagic or ischaemic

235
Q

What are the signs of an anterior cerebral artery stroke?

A
  1. Lower limb weakness and loss of sensation to lower limb
  2. Gait apraxia – cant initate walking
  3. Incontiencne
  4. Drowsiness
  5. Decrease in spontaneous speech
236
Q

What are the signs of a middle cerebral artery stroke?

A
  1. Upper limb weakness and loss of sensation to upper limb
  2. Hemianopia
  3. Aphasia
  4. Dysphasia
  5. Facial drop
237
Q

What are the signs of a Posterior cerebral artery stroke?

A
  1. Visual field defects
  2. Ccortical blindness
  3. Visual agnosia – an inability to interpret visual info
  4. Prosopagnosia – an inability to recognise face
  5. Dyslexia and Unilateral headache
238
Q

What is the treatment for ischaemic stroke?

A

Thrombolysis –> Alteplase IV to break up clot

239
Q

What is the treatment for haemorrhagic stroke?

A

Surgery to lower pressure and surgical clipping/

240
Q

What is the non pharmacological treatment of stroke?

A
  1. Specialised stroke units
  2. Swallowing and feeding help
  3. Physio and home modifications.
241
Q

What is epilepsy?

A

Tendency to have seizures

242
Q

What is a seizure?

A

a convulsion caused by paroxysmal discharge of cerebral neurones.

  • Abnormality and excessive excitability of neurones.
243
Q

What is 5 causes of transient loss of consciousness?

A
  1. Syncope
  2. Epileptic seizures
  3. Non-epileptic seizures
  4. Intoxication
  5. Ketoacidosis/hypoglycaemia
  6. Trauma
244
Q

What are the causes of epilepsy?

A
  1. Flashing lights
  2. Cerebrovascular disease
  3. Genetic predisposition
  4. CNS infection e.g. meningitis
  5. Trauma
245
Q

What is an epileptic seizure?

A

excessive unsychronised neuronal changes in the brain that cause paroxysmal changes in behaviour, sensation or cognitive processes

246
Q

What are the signs of an epileptic seizure?

A
  1. 30-120s in duration
  2. Positive symptoms e.g. tingling and movement
  3. Tongue biting
  4. Head turning
  5. Muscle pain
247
Q

What are the stages of a seizure?

A
  1. Prodromal – often emotional signs
  2. Aura
  3. Ital
  4. Post-ictal –> drowsy and confused
248
Q

What is the cause of subarachnoid haemorrhage?

A

Life threatening stroke caused by bleeding into the space surrounding the brain

249
Q

What is the symptom associated with subarachnoid haemorrhage?

A

Thunderclap headache associated –> maximum severity within seconds

250
Q

What is the investigation in suspected subarachnoid haemorrhage?

A
  • CT of the head

- Cerebral angiography

251
Q

What is the treatment of subarachnoid haemorrhage?

A
  1. Resuscitation
  2. Nimodipine (CCB)
  3. Early intervention and close monitoring improve prognosis
252
Q

What is an intracerebral haemorrhage?

A

Intracerebral hemorrhage (ICH) is caused by bleeding within the brain tissue itself — a life-threatening type of stroke.

253
Q

What are the primary causes of intracerebral haemorrhage?

A
  1. Hypertension –> Berry or Charcot bouchard aneurysms –> rupture
  2. Lobar (amyloid angiopathy)
254
Q

What are the secondary causes of intracerebral haemmorhage?

A
  1. Tumour
  2. AV malformations
  3. Cerebral aneurysm
  4. Anticoagulants e.g. warfarin
  5. Haemorrhagic transformation infarct
255
Q

What is a complication of a charcout bouchard aneurysm?

A

Rupture, thrombosis and leakage

256
Q

If a bleed is present in the

Pons
Cerebellum
Basal ganglia

What is the likely cause?

A

Hypertension

257
Q

What is the anticoagulant treatment for intracerebral haemorrhage?

A
  1. Check warfarin consider reversal with Vit K

2. If low platelets –> platelet transfusion

258
Q

What are the 3 intracranial haemorrhages?

A
  1. Extra-dural
  2. Sub-Dural
  3. Sub-arachnoid
259
Q

What is the cause of a subarachnoid haemorrhage?

A

can be caused by a rupture of a berry aneurysm around the circle of Willis

260
Q

What are the symptoms of a subarachnoid haemorrhage?

A
  1. Sudden onset of thunderclap headaches
  2. Photophobia
  3. Reduced consciousness
  4. Neck stiffness
  5. Nausea and vomiting
261
Q

What investigations of a SA haemorrhage?

A
  1. CT scan of Head –> blood in the sulci
  2. Lumbar puncture
  3. MRA
262
Q

What is the treatment of a SA haemorrhage?

A
  1. Bed rest and BP control
  2. CCB to prevent cerebral artery spasm
  3. IV saline
263
Q

How long should you wait for before doing a lumbar puncture in suspected SAH?

264
Q

Why does the CSF look like in a patient with SAH?

A

Hb needs to break down and the CSF become yellow –> sign of xanthochromia – bleeding into the SA space.

265
Q

What is the cause of SDH?

A

can be caused by a head injury causing venous rupture

266
Q

What is the history of SDH?

A
  • Latent period after injury –> 8/10 weeks later clot breaks down = rise in oncotic pressure
  • Water is sucked up into the haematoma and signs and symptoms soon develop
267
Q

What are the symptoms of SDH?

A
  1. Headache
  2. Drowsiness
  3. Confusion
268
Q

What is the treatment for SDH?

A
  1. Surgical Removal
269
Q

Who is at risk of SDH?

A

Groups at risk  Elderly people, alcoholics and shaken babies

270
Q

Why are elderly people and alcoholics at greater risk of SDH?

A

Elderly people and alcoholics are at a greater risk due to cerebral atrophy which increases tension of the cerebral veins.

271
Q

What is the cause of an extradural haemorrhage?

A

Trauma to the temporal bone causing bleeding from the middle meningeal artery.

272
Q

What is the purpose of the ventricles?

A

Get rid of CSF to prevent a rise in inter-cranial pressure.

273
Q

What are the signs of an extradural haemorrhage?

A

GCS will drop suddenly and accompanied with a rapid deterioration of consciousness

274
Q

What is the treatment of an extradural haemorrhage?

A

Immediate surgical drainage.

275
Q

How many strokes are down to intracerebral haemorrhage?

276
Q

What is the difference in presentation of a subdural and extradural haemorrhage?

A
  1. Time frame – extradural symptoms are more acute
  2. GCS – subdural GCS will fluctuate whereas GCS will drop suddenly in someone with extradural haematoma
  3. CT – extradural haematoma will have a rounder more contained appearance

Phase 2a Sheffield Medicine (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions