Neurology Flashcards

Question 1

Q

what do oligodendrocytes do?

Answer

A

myelinate axons in the brain (CNS)

Question 2

Q

what do Schwann cells do?

Answer

A

myelinate axons in the rest of the body (PNS)

Question 3

Q

what are afferents?

Answer

A

axons taking information towards the CNS e.g. sensory fibres

Question 4

Q

what are efferents?

Answer

A

axons taking information to another site from the CNS e.g. motor fibres

Question 5

Q

what are the functions of the frontal lobe?

Answer

A

voluntary movement on opposite side of body
frontal lobe of dominant hemisphere controls speech (Broca’s area) and writing
intellectual functioning, thought processes, reasoning and memory

Question 6

Q

what are the functions of the parietal lobe?

Answer

A

receives and interprets sensations, including pain, touch, pressure, size and shape and proprioception

Question 7

Q

what are the functions of the temporal lobe?

Answer

A

understanding the spoken word (Wernicke’s area), sounds, memory and emotion

Question 8

Q

what are the functions of the occipital lobe?

Answer

A

understanding visual images and meaning of written words

Question 9

Q

what is the CSF produced by?

Answer

A

CSF is produced by ependymal cells in the choroid plexuses of the lateral ventricles (mainly)

Question 10

Q

what is the passage of CSF?

Answer

A

from the lateral ventricles it travels to the 3rd ventricle via the interventricular foramen and then from the 3rd ventricle it travels to the 4th ventricle via the cerebral aqueduct (Aqueduct of Sylvius)
from the 4th ventricle it communicates with the subarachnoid space via the median foramen of Magendie and the two lateral foramens of Luschka

Question 11

Q

what is the Aqueduct of Sylvius?

Answer

A

cerebral aqueduct connecting the 3rd and 4th ventricles

located dorsal to the pons and ventral to the cerebellum
the cerebral aqueduct is surrounded by the periaqueductal grey

Question 12

Q

what is the interventricular foramen?

Answer

A

channels that connect the paired lateral ventricles with the 3rd ventricle at the midline of the brain

Question 13

Q

what is the foramen of Monro?

Answer

A

channels that connect the paired lateral ventricles with the 3rd ventricle at the midline of the brain

Question 14

Q

what is the foramen of Magendie?

Answer

A

drains CSF from the fourth ventricle into the cisterna magna

Question 15

Q

what is the foramen of Luschka?

Answer

A

opening in each lateral extremity of the lateral recess of the 4th ventricle of the human brain, which also has a single median aperture
allows CSF to flow from the ventricles into the subarachnoid space

Question 16

Q

how is CSF absorbed?

Answer

A

CSF is then absorbed via arachnoid granulations

Question 17

Q

what is hydrocephalus?

Answer

A

abnormal accumulation of CSF in ventricular system

* often due to a blocked cerebral aqueduct

Question 18

Q

what does the sympathetic system supply?

Answer

A

supplies visceral organs and structures of superficial body regions
contains more ganglia than the the parasympathetic division

Question 19

Q

what are the effects of the sympathetic system?

Answer

A

increases heart rate
increases force of contractions in the heart
vasoconstriction
bronchodilaton
reduces gastric motility
sphincter contraction
decreased gastric secretions
male ejaculation

Question 20

Q

what are the parasympathetic cranial nerves? what do they supply?

Answer

A

oculomotor nerve CN3 to pupil
facial nerve CN7 to salivary glands
glossopharyngeal nerve CN9 for swallowing reflex
vagus nerve CN10 to thorax and abdomen

Question 21

Q

what does the parasympathetic system innervate?

Answer

A

organs of the head, neck, thorax and abdomen

Question 22

Q

what are the effects of the parasympathetic system?

Answer

A

decreases heart rate
decrease force of contraction
vasodilation
bronchoconstriction
increases gastric motility
sphincter relaxation
increased gastric secretions
male erection

Question 23

Q

what are upper motor neurons?

Answer

A

the descending pathways and neurones that originate in the motor cortex
control the activity of the lower motor neurones

Question 24

Q

what are lower motor neurons? what are they also known as?

Answer

A

alpha motor neurones that directly innervate skeletal muscle that have cell bodies lying in the grey matter of the spinal cord and brainstem

Question 25

Q

what is spasticity? when is it seen?

Answer

A

increased muscle tone
muscles do not develop increased tone until they are stretched a bit, and after a brief increase in tone, the contraction subsides for a short time
the period of ‘give’ occurring after resistance is called the clasp-knife phenomenon, where someone bends the limb of a patient, initially there is some resistance but after a certain point resistance falls dramatically
seen in Parkinson’s

Question 26

Q

what is rigidity?

Answer

A

increased muscle contraction is continuous and the resistance to passive stretch is constant

Question 27

Q

what does the vertebral column consist of? how many cervical, thoracic, lumbar and sacral vertebra are there?

Answer

A

7 Cervical vertebra
12 Thoracic vertebra
5 Lumbar vertebra (fused)
4 Coccyx vertebra (fused)

Question 28

Q

what do the spinal nerves consist of? how many cervical, thoracic, lumbar and sacral nerves are there?

Answer

A

8 cervical nerves
12 thoracic nerves
5 lumbar nerves
5 sacral nerves
1 coccyx nerve

Question 29

Q

where do spinal nerves exit from the cord?

Answer

A

cervical segments: around 1 vertebra higher than their corresponding vertebra (except C8 which exits below a vertebra)
thoracic segments: around 1-2 vertebra below their corresponding vertebra
lumbar segments: 3-4 vertebra below their corresponding vertebra
sacral segments: around 5 vertebra below

Question 30

Q

what is a dermatome?

Answer

A

area of skin supplied by a single spinal nerve

Question 31

Q

what is the sensory innervation of the hand?

Answer

A

palmar:
- little finger and medial half of ring finger (ulnar nerve, C8)
- lateral half of ring finger, middle finger, index finger and medial half of thumb (median nerve, C7)
- lateral half of thumb (radial nerve, C6)

dorsal:

thumb, proximal half of index, middle finger and lower 1/4 of the ring finger (radial nerve, C6)
distal half of index, middle finger and upper 1/4 of ring finger (median nerve, C7)
half of ring finger and all of little finger (ulnar nerve, C8)

Question 32

Q

what are the different dermatomes and what do they supply?

Answer

A

C4: clavicle
T4: nipples
T1: medial arm
T10: umbilicus
L4: knee
S4: perianal area
S5: anus

Question 33

Q

what is a myotome?

Answer

A

a volume of muscle supplied by a single spinal nerve

Question 34

Q

what are the motor tracts?

Answer

A

lateral corticospinal tract
rubrospinal tract
olivospinal tract
vestibulospinal tract
tactospinal tract
anterior corticospinal tract

Question 35

Q

what are the sensory tracts?

Answer

A

fasiculus gracilis
fasiculus cuneatus
posterolateral tract
intersegmental tract
posterior spinocerebellar tract
lateral spinothalamic tract
anterior spinocerebellar tract
spino-olivary tract
spinorectal tract
anterior spinothalamic tract

Question 36

Q

what are the ascending tracts?

Answer

A

sensory
dorsal/medial lemniscal columns
spinothalamic tract
spinocerebellar tract

Question 37

Q

what are features of the DCML tract?

Answer

A

dorsal root ganglion is 1st order neuron
fasiculus cuneatus and fasiculus gracilis
carries proprioception, vibration and fine touch (via Ruffini endings, Merkel discs, Pacinian corpuscles)
fasiculus cuneatus is lateral and carries information from the upper body to the cuneate tubercle in the medulla
fasiculus gracilis is medial and carries information from the lower body to the gracile tubercle in the medulla
decussation of internal arcuate fibres in the medulla to become the medial lemniscus
2nd order neuron is from the midbrain to thalamus (VPLN)
3rd order neuron is from the thalamus (VPLN) to the somatosensory cortex (through internal capsule and corona radiata)

Question 38

Q

what is the function of the spinothalamic tract?

Answer

A

carries pain, temperature (lateral) and crude touch (anterior) information
1st order neurones arise from sensory receptors in the periphery and enter spinal cord and ascend 1-2 vertebral levels then synapse at the substantia gelatinosa
2nd order neurones synapse with 1st order neurones and then decussate within the spinal cord, then form anterior/lateral tracts, and synapse in the thalamus (VPL)
3rd order neurones ascend from the VPL, travel through the internal capsule and terminate at the sensory cortex

Question 39

Q

what are the pathways in the spinocerebellar tracts? what are their functions?

Answer

A

posterior spinocerebellar tract: carries proprioceptive information from the lower limbs to the ipsilateral cerebellum (from muscle spindle and golgi tendon organs)
cuneocerebellar tract: carries proprioceptive information from the upper limbs to the ipsilateral cerebellum (from muscle spindle and golgi tendon organs)
anterior spinocerebellar tract: carries proprioceptive information from the lower limbs, decussates twice and terminates in ipsilateral cerebellum (from golgi tendon organs)
rostral spinocerebellar tract: carries proprioceptive information from the upper limbs to the ipsilateral cerebellum (from golgi tendon organs)

Question 40

Q

what is the pyramidal pathway?

Answer

A

include the corticobulbar tract and the corticospinal tract
aggregations of efferent nerve fibres from the UMNs that travel from the cerebral cortex and terminate in the brainstem (corticobulbar) or spinal cord (corticospinal)
involved in the control of motor functions of the body and face

Question 41

Q

what is the pathway of the corticobulbar tract?

Answer

A

originates in the primary motor cortex of the frontal lobe, superior to the lateral fissure and rostral to the central sulcus in the precentral gyrus (Brodmann area 4)
descends through the corona radiata and genu of the internal capsule
in the midbrain, the internal capsule becomes the cerebral peduncles
the white matter is located in the ventral portion of the cerebral peduncles, called the crus cerebri
corticobulbar fibres exit at the appropriate level of the brainstem to synapse on the LMNs of the cranial nerves
fibres also end in the sensory nuclei of the brainstem including gracile nucleus, cuneate nucleus, solitary nucleus and all trigemnial nuclei

Question 42

Q

what does the corticobulbar tract innervate?

Answer

A

directly innervates nuclei for cranial nerves V, VII, IX and XII
contributes to motor regions of cranial nerve X in the nucleus ambiguus
most innervate motor neurones bilaterally, except for the UMNs for the facial nerve and hypoglossal nerve (receive contralateral innervation)

Question 43

Q

what is the pathway of the corticospinal tract?

Answer

A

receive input from the primary motor cortex, premotor cortex, supplementary motor area and the somatosensory area
converge and descend through the internal capsule, through the crus cerebri of midbrain, the pons and into the medulla
then the tract divides into the lateral CST (decussates and becomes contralateral) and the anterior CST (remains ipsilateral, then decussates in spinal cord)
neurones then terminate on the ventral horn (anterior CST only supplies cervical and upper thoracic levels)

Question 44

Q

what is the vestibulospinal tract?

Answer

A

medial and lateral pathways
arise from vestibular nuclei (receive input from organs of balance; CN8)
send information to spinal cord and control balance and posture by innervating anti-gravity muscles (flexors of arm and extensors of leg) via LMNs
ipsilateral

Question 45

Q

what is the tectospinal tract?

Answer

A

begins in the superior (visual) colliculus and receives information from the optic nerves
terminate at the cervical levels of spinal cord
coordinates movements of head in relation to visual stimuli
contralateral

Question 46

Q

what is the rubrospinal tract?

Answer

A

originates from the red nucleus (midbrain)
facilitates flexors and inhibits extensors; controls fine hand movements
decussates at the midbrain thus is contralateral

Question 47

Q

what is the pathophysiology of Brown-Sequard syndrome?

Answer

A

ipsilateral weakness/UMN signs below the lesion due to lateral CST lesion
ipsilateral loss of proprioception, light touch and vibration sense below the lesion due to DCML lesion
contralateral loss of pain and temperature sensation below the lesion due to lesions to lateral spinothalamic tract

Question 48

Q

what are the component fibres, structures innervated, function and skull exit point of the olfactory CN?

Answer

A

component fibres: sensory/special
structures innervated: olfactory epithelium
function: olfaction
skull exit point: cribriform plate

Question 49

Q

what are the component fibres, structures innervated, function and skull exit point of the optic CN?

Answer

A

component fibres: sensory/special
structures innervated: retina
function: vision; pupillary light reflex
skull exit point: optic canal

Question 50

Q

what are the component fibres, structures innervated, function and skull exit point of the oculomotor CN?

Answer

A

component fibres: motor-somatic and parasympathetic
structures innervated:
superior, inferior and medial rectus muscle, inferior oblique muscle, levator palpabrae superioris, sphincter pupillae and ciliary muscle of eyeball
function: movement of eyeball, elevation of upper eyelid, pupillary constriction and accomodation
skull exit point: superior orbital fissure

Question 51

Q

what are the component fibres, structures innervated, function and skull exit point of the trochlear CN?

Answer

A

component fibres: motor/somatic
structures innervated: superior oblique muscle
function: movement of eyeball
skull exit point: superior orbital fissure

Question 52

Q

what are the component fibres, structures innervated, function and skull exit point of the opthalamic CN?

Answer

A

component fibres: sensory/somatic
structures innervated: face, scalp, cornea, nasal and oral cavities
function: general sensation
skull exit point: superior orbital fissure

Question 53

Q

what are the component fibres, structures innervated, function and skull exit point of the maxillary CN?

Answer

A

component fibres: sensory/somatic
structures innervated: muscles of mastication, sub-mandibular, sublingual and parotid glands
function: opening and closing of mouth
skull exit point: foramen rotundum

Question 54

Q

what are the component fibres, structures innervated, function and skull exit point of the mandibular CN?

Answer

A

component fibres: motor/branchial
structures innervated: tensor tympani
function: tension on tympanic membrane
skull exit point: foramen ovale

Question 55

Q

what are the component fibres, structures innervated, function and skull exit point of the abducens CN?

Answer

A

component fibres: motor/somatic
structures innervated: lateral rectus muscle
function: movement of eyeball
skull exit point: superior orbital fissure

Question 56

Q

what is the function, structures innervated and skull exit point of the sensory facial nerve?

Answer

A

structures innervated: anterior 2/3 of tongue
function: taste
skull exit point: internal acoustic meatus

Question 57

Q

what is the structures innervated, function and skull exit point of the motor facial nerve?

Answer

A

structures innervated: muscles of facial expression
function: facial movement
skull exit point: internal acoustic meatus

Question 58

Q

what is the structures innervated, function and skull exit point of the parasympathetic facial nerve?

Answer

A

structures innervated: salivary and lacrimary glands
function: salivation and lacrimation
skull exit point: internal acoustic meatus

Question 59

Q

what are the component fibres, structures innervated, function and skull exit point of the vestibulocochlear CN?

Answer

A

component fibres: sensory; special
structures innervated: vestibular apparatus and cochlea
function: position and movement of head and hearing
skull exit point: internal acoustic meatus

Question 60

Q

what are the structures innervated, function and skull exit point of the sensory glossopharyngeal CN?

Answer

A

structures innervated: pharynx, posterior 1/3 of the tongue, eustachian tube, middle ear, carotid body, carotid sinus
function: general sensation, taste, chemoreception, baroreception
skull exit point: jugular foramina

Question 61

Q

what are the structures innervated, function and skull exit point of the motor glossopharyngeal CN?

Answer

A

structures innervated: stylopharyngeus muscle
function: swallowing
skull exit point: jugular foramina

Question 62

Q

what are the structures innervated, function and skull exit point of the parasympathetic glossopharyngeal CN?

Answer

A

structures innervated: parotid salivary gland
function: salivation
skull exit point: jugular foramina

Question 63

Q

what are the structures innervated, function and skull exit point of the sensory vagus CN?

Answer

A

structures innervated: pharynx, larynx, trachea, oesophagus, thoracic and abdominal viscera, aortic bodies, aortic arch
function: general sensation, visceral sensation, chemoreception, baroreception
skull exit point: jugular foramina

Question 64

Q

what are the structures innervated, function and skull exit point of the motor vagus CN?

Answer

A

structures innervated: soft palate, pharynx, larynx, oesophagus
function: speech, swallowing
skull exit point: jugular foramina

Answer 65

A

structure innervated: thoracic and abdominal viscera
function: innervation of cardiac muscle, innervation of smooth muscle, respiratory and GI tracts
skull exit point: jugular foramina

Answer 66

A

component fibres: motor/somatic
structures innervated: sternocleidomastoid and trapezius muscles
function: movement of head and shoulders
skull exit point: jugular foramina

Answer 67

A

component fibres: motor/somatic
structures innervated: intrinsic and extrinsic muscles of the tongue
function: movement of tongue
skull exit point: hypoglossal canal

Answer 68

A

midbrain: 3,4
pons: 5,6,7,8
medulla: 9,10,11,12

Answer 69

A

damage to this area can result in expressive aphasias (difficulty forming words or sentences)
they will understand what you are saying and know what they want to say but cannot express the words into meaningful language

Answer 70

A

damage to this area results in comprehension/receptive aphasias (difficulty understanding spoken or written language, even though their hearing and vision are not impaired)
they tend to have fluent speech but they may scramble words so that their sentences make no sense, often adding unnecessary words or made-up words

Answer 71

A

the most common type of intercranial aneurysm
most common at the anterior cerebellar artery and anterior communicating artery junction
produces a subarachnoid haemorrhage, resulting in a thunderclap headache

Answer 72

A

one of the dural venous sinuses
creates a cavity called the lateral sellar compartment
chamber of venous blood
contains CN3, 4, 5.1, 5.2, 6

Answer 73

A

fibres from the nasal portion of the retina (carrying the temporal fibres) cross at the optic chiasm located anterior to the pituitary infundibulum
optic tracts carry the fibres posterolaterally around the cerebral peduncles to terminate at the lateral geniculate bodies of the thalamus
fibres from the temporal portion of the retina (carrying the nasal fibres) do the same as above
after the lateral geniculate body, the optic radiations split into two; the fibres carrying information from the inferior portions of the retina (superior visual fields) travel by looping laterally through the temporal lobe to the visual cortex (Meyer’s loop)
the fibres carrying information from the superior portions of the retina (inferior visual fields) travel by looping superiorly through the parietal lobe to the visual cortex (Baum’s loop)

Answer 74

A

medial rectus
lateral rectus
superior oblique
inferior oblique
superior rectus
inferior rectus
levator palpebrae supeioris

Answer 75

A

pulls the eye medially (adduction)

Answer 76

A

pulls the eye laterally (abduction)

Answer 77

A

intorsion (top of eye rotating towards the midline)

- depresses the eye medially

Answer 78

A

extorsion (top of eye rotating away from the midline)

- elevates the eye medially

Answer 79

A

pulls the eye down and medially

- also rotates it

Answer 80

A

lifts upper eyelid

Answer 81

A

medial rectus, inferior oblique, superior rectus, inferior rectus

Answer 82

A

lateral rectus

Answer 83

A

superior oblique

Answer 84

A

levator palpebrae supeioris (also have sympathetic nerve supply - open eyelid in fear)
loss of function = ptosis

Answer 85

A

LR6SO4

lateral rectus = CN6
superior oblique = CN4
all the rest = CN3

Answer 86

A

pulls the eye up and medially

- also rotates it

Answer 87

A

allows us to anaesthetise the lower part of body so brain will still control breathing
tube inserted below L1, outside the dura mater and local anaesthetic administered into the epidural space; it will diffuse into the dorsal root ganglia on sensory nerves
will stop the cell bodies of the sensory neurones from working and thus no pain is transmitted
purposely use a blunt needle since don’t want to go into the CSF - if it does then anaesthetic will travel up to the brain and cause respiratory distress
if dose is just right then since the cell bodies of motor neurones will not be affected; ideal for pregnancy since muscles are required but do not want sensation and proprioception

Answer 88

A

best way to sample CSF
done at L3/4 or L4/L5
use very sharp needle since want to penetrate dura and extract CSF, then use plunger to aspirate

Answer 89

A

small response = axon loss

* slow response = myelin loss (demyelination)

Answer 90

A

use a needle to detect the electrical activity from muscle
records the activity of individual motor units
can look at big motor units for signs of nerve/motor neurone pathology
can look at small motor units for signs of myopathy
EMG can detect myopathies, nerve conduction studies will be normal even in myopathy but EMG will not
EMG will detect myaesthenia gravis

Answer 91

A

small response = axonal neuropathy; not treatable

* slow response = demyelinating neuropathy; treatable

Answer 92

A

focal nerve entrapment, generalised peripheral neuropathy, myopathy and motor neurone disease

Answer 93

A

runs over the petrous apex of the temporal bone
if there is fracture or inflammation then CN3 can get pushed against the bone resulting in a fixed dilated pupil (telltale sign of CN3 under pressure)

Answer 94

A

CN3 under pressure; fracture or inflammation of the petrous apex of the temporal bone

Answer 95

A

ataxia - loss of full control of body movements - limb unsteadiness
nystagmus - rapid eye movements
deficit is on same side as cerebellar lesion (ipsilateral)

Answer 96

A

• periaqueductal grey matter on the floor of the 4th ventricle
• responsible for:
- alertness
- sleep/wake
- REM and non REM sleep
- respiratory centre
- cardiovascular centre

Answer 97

A

superior and inferior opthalamic veins, the middle superficial cerebral veins and a dural venous sinus

Answer 98

A

O TOM CAT - say trochlear twice
• Oculomotor nerve (3)
• Trochlear nerve (4)
• Opthalmic trigeminal (5.1)
• Maxillary trigeminal (5.2)
• Carotid (internal)
• Abducens (6) - only one going medially
• Trochlear nerve (4)

Answer 99

A

pupils
corneal reflex
caloric vestibular reflex
cough reflex
gag reflex
respirations
response to pain

Answer 100

A

GCS; glasgow coma scale, measure of level of consciousness
look at lateralising signs (to check what hemisphere is damaged)
look at pupils for signs of raised ICP
monitor vital signs

Answer 101

A

• score adds to 14 and consists of 3 categories:
- motor response (most important)
- verbal response
- eye opening response
• inaccurate within one hour of event

Answer 102

A

IV mannitol (diuretic) to reduce oedema and ICP
management of seizures e.g diazepam for status epilepticus
intubation usually done if GCS is less than 8
neurosurgery (ICP monitor insertion or burrholes/craniectomy)
suture scalp lacerations before moving to CT

Answer 103

A

a brief episode of neurological dysfunction due to temporary focal cerebral ischaemia without infarction
- symptoms generally resolve within 24 hours

Answer 104

A

15% of first strokes are preceded by TIA, they are also a foreshadowing of an MI
more common in males than females
black ethnicity people are at greater risk due to their hypertension and atherosclerosis predisposition

Answer 105

A

small vessel occlusion
atherothromboembolism from the carotid artery is the main cause
cardioembolism resulting in microembolism (mural thrombus post-MI or AF, valve disease, prosthetic valve)
hyperviscosity (polycythaemia, sickle cell anaemia, raised WCC, myeloma)
can result from hypoperfusion; most important to consider in younger people (cardiac dysrhythmia, postural hypotension, atherosclerosis)

Answer 106

A

risk increases with age
hypertension
smoking
diabetes
heart disease - valvular, ischaemic or atrial fibrillation
past TIA
raised packed cell volume (PCV)
peripheral arterial disease
polycythaemia vera
combined oral contraceptive pill (since increase risk of clots)
hyperlipidaemia
excess alcohol
clotting disorder
vasculitis e.g. SLE, giant cell arteritis is rare risk factor

Answer 107

A

the commonest cause of a TIA is cerebral ischaemia resulting in a lack of O2 and nutrients to the brain resulting in cerebral dysfunction, however in a TIA this period of ischaemia is short-lived, with symptoms usually only lasting a maximum of 5-15 minutes after onset, and then resolves with before irreversible cell death occurs
symptoms that gradually progress suggest a different pathology such as demyelination, tumour or migraine

Answer 108

A

sudden loss of function, usually lasting for minutes only, with complete recovery and no evidence of infarction on imaging
site of TIA is often suggested by symptoms
90% of TIA’s affect the anterior circulation (carotid artery)
10% affect the posterior circulation (vertebrobasilar artery)

Answer 109

A

supplies the frontal and medial part of the cerebrum
occlusion may cause a weak, numb contralateral leg +/- similar, if milder, arm symptoms
hemiparesis
hemisensory disturbance
dysphasia (language impairment)
amaurosis fugax

Answer 110

A

sudden transient loss of vision in one eye
described as a; “curtain coming down vertically into field of vision”
occurs due to the temporary reduction in the retinal, opthalmic or ciliary blood flow leading to temporary retinal hypoxia
TIA causing this is often the first clinical evidence of an ICA stenosis; warning sign of an imminent ICA territory stroke

Answer 111

A

diplopia
vertigo
vomiting
choking and dysarthria (unclear articulation of speech but understandable)
ataxia - no control of body movement
hemisensory loss
hemianopia vision loss
loss of consciousness (rare)
transient global amnesia - episode of confusion/amnesia lasting several hours, followed by complete recovery
tetraparesis

Answer 112

A

until there is a full recovery it is impossible to differentiate from a stroke
hypoglycaemia, migraine aura (symptoms spread and intensify over minutes, often with visual scintillations), focal epilepsy (since limb shaking can occur in a TIA)
intracranial lesion - tumour or subdural haemotoma
syncope due to arrhythmia
Todd’s paralysis (transient weakness of arm, hand or leg after a seizure)
retinal or vitreous haemorrhage
giant cell arteritis

Answer 113

A

transient weakness of arm, hand or leg after a seizure, can last up to 48 hours

Answer 114

A

raised ESR, thickening and tenderness of temporal artery

* monocular, temporary visual impairment normally presents

Answer 115

A

often based solely on its description
bloods
carotid artery doppler ultrasound to look for stenosis/atheroma
MRI/CT angiography if stenosis to determine extent
ECG (look for AF or evidence of MI/ischaemia)
CT or diffusion weighted MRI
echocardiogram/cardiac monitoring to assess for a cardiac cause

Answer 116

A

FBC - look for polycythaemia
ESR - will be raised in vasculitis
glucose - to see if hypoglycaemic
creatinine, electrolytes
cholesterol

Answer 117

A

• age > 60yrs = 1
• blood pressure > 140/90mmHg = 1
• clinical features:
- unilateral weakness = 2
- speech disturbance without weakness = 1
• duration of symptoms:
- symptoms lasting more than 1hr = 2
- symptoms lasting 10-59mins = 1
• diabetes = 1

Answer 118

A

score greater than 6 strongly predicts a stroke and should be referred to a specialist immediately
score greater than 4 should be assessed by a specialist within 24hours
all patients with a suspected TIA should be seen within 7 days

Answer 119

A

people are also at high risk of an early stroke if they have:
• atrial fibrillation
• more than 1 TIA in one week
• TIA whilst on an anticoagulant

Answer 120

A

assess risk factor for a stroke using the ABCD2 score
antiplatelet drugs
anticoagulant if they have AF, mitral stenosis or recent big septal MI e.g. warfarin
statin long term
control cardiovascular risk factors
do not drive for at least 4 weeks following a TIA

Answer 121

A

aspirin immediately and dipyridamole (to increase cAMP and decrease thromboxane A2) for two weeks then lower dose
P2Y12 inhibitor longterm e.g. clopidogrel

Answer 122

A

antihypertensives such as ACE-inhibitor e.g. ramipril or angiotensin receptor blocker e.g. candesartan
improve diet, stop smoking

Answer 123

A

syndrome of rapid onset of neurological deficit caused by focal, cerebral, spinal or retinal infarction
characterised by rapidly developing signs of focal or global disturbance of cerebral functions, lasting for more than 24hrs or leading to death

Answer 124

A

stroke, whether ischaemic or haemorrhagic, is the major neurological disease of our time
3rd most common cause of death in high-income countries; 11% of all deaths in UK
leading cause of adult disability worldwide
stroke rates are higher in Asian and black African populations than in Caucasians
uncommon in those under 40
incidence increases with age
more common in males than females
incidence is falling due to more vigorous approach to risk factors in primary care i.e. statin use and control of BP

Answer 125

A

ischaemic/infarction accounts for 80% of strokes
haemorrhagic accounts for 17% of strokes
other causes account for about 3%
young people
elderly

Answer 126

A

small vessel occlusion/thrombosis in situ
cardiac emboli from AF, MI or infective endocarditis
large artery stenosis
atherothromboembolism
hypoperfusion, vasculitis, hyperviscosity (polycythaemia and sickle cell)
hypoperfusion/watershed stroke

Answer 127

A

hypoperfusion/watershed stroke: where there is a sudden BP drop by more than 40mmHg, then there is low cerebral blood flow, leading to global ischaemia and ‘watershed infarcts’ in vulnerable areas of cortex between boundaries of different arterial territories; seen in sepsis

Answer 128

A

trauma
aneurysm rupture
anticoagulation
thrombolysis
carotid artery dissection
subarachnoid haemorrhage

Answer 129

A

vasculitis
thrombophilia
subarachnoid haemorrhage
carotid artery dissection - spontaneous, or from neck trauma
venous sinus thrombosis

Answer 130

A

very rare (only 1%)
thrombosis within intracranial venous sinuses, such as the superior sagittal sinus, or in cortical veins, may occur in pregnancy, hypercoaguable states and thrombotic disorders or with dehydration or malignancy
cortical infarction, seizures and raised intracranial pressure result

Answer 131

A

thrombosis in situ
athero-thromboembolism
heart emboli e.g. AF, infective endocarditis or MI
CNS bleed
sudden BP drop by more than 40mmHg
vasculitis
venous sinus thrombosis

Answer 132

A

male
black or asian
hypertension
past TIA
smoking
diabetes mellitus
increasing age
heart disease (valvular, ischaemic)
alcohol
polycythaemia, thrombophilia
AF/stasis of blood in poorly contracting atria leads to thrombus formation
hypercholesterolaemia
combine oral contraceptive pill
vasculitis
infective endocarditis

Answer 133

A

arterial disease and atherosclerosis is the main pathological process
thrombosis occurs at site of atheromatous plaque in carotid/vertebral/cerebral arteries
large artery stenosis acts as an embolism source rather than occluding the vessel
lipohyalinosis
cardioembolism
venous sinus thrombosis

Answer 134

A

an occlusive vasculopathy known as lipohyalinosis that is a consequence of hypertension results in small infarcts known as ‘lacunes’ and/or the gradual accumulation of diffuse ischaemic change in deep
white matter

Answer 135

A

AF
cardiac valve disease
infective vegetations due to endocarditis
mural thrombosis from damaged ventricle
fat emboli after long bone fracture
hypoperfusion

Answer 136

A

hypertension resulting in micro aneurysm rupture (Charcot-Bouchard aneurysms)
cerebral amyloid angiopathy (deposition of beta amyloid leading to lobar intercerebral haemorrhage)
space occupying lesion e.g. tumour - rare
carotid/vertebral artery dissection in young adults due to neck pain, trauma or neck manipulation

Answer 137

A

leg weakness (more likely than arm weakness since more of leg in ACA)
sensory disturbances in the legs
gait apraxia
truncal ataxia; patients can’t sit or stand unsupported and tend to fall backwards
incontinence
drowsiness, since part of consciousness is in the frontal lobe
akinetic mutism (decrease in spontaneous speech, stuporous state)

Answer 138

A

contralateral arm and leg weakness
contralateral sensory loss
hemianopia
aphasia (inability to understand or produce speech)
dysphasia (deficiency in speech generation)
facial droop

Answer 139

A

• contralateral homonymous hemianopia
• cortical blindness (eye healthy, but brain issue
causing blindness)
• visual agnosia (cannot interpret visual information, but can see)
• prosopagnosia (cannot see faces)
• colour naming and discriminate problems
• unilateral headache - rare in ischaemic stroke, so if you see headache then think PCA

Answer 140

A

more catastrophic due to wide region supplied
likely to get ‘locked in’ in these strokes
motor deficits such as hemiparesis or tetraparesis and facial paralysis
dysarthria (unclear speech articulation) and speech impairment
vertigo, nausea and vomiting
visual disturbance
altered consciousness

Answer 141

A

small subcortical strokes e.g. midbrain, internal capsule, one of:

unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three
pure sensory loss
ataxic hemiparesis (cerebellar and motor symptoms)
in general only 1 modality tends to be affected

Answer 142

A

intracerebral haemorrhage is more often associated with severe headache or coma (signs of raised ICP due to blood forming a space-occupying lesion)
patients on oral anticoagulants should be assumed to have had a haemorrhage unless it is proved otherwise

Answer 143

A

always exclude hypoglycaemia as a cause of sudden onset neurological syndrome
hypoglycaemia, migraine aura (symptoms spread and intensify over minutes, often with visual scintillations), focal epilepsy (since limb shaking can occur in a TIA)
intracranial lesion; tumour or subdural haemotoma
syncope due to arrhythmia

Answer 144

A

urgent CT head/MRI head before treatment
pulse, BP and ECG (look for AF)
bloods (look for thrombocytopenia, polycythaemia and hypoglycaemia)

Answer 145

A

• urgent if suspected cerebellar stroke, unusual presentation, high risk of haemorrhage (low GCS and
signs of raised ICP)
• used to rule out haemorrhagic stroke before starting thrombolysis
• infarction is seen as a low density lesion, subtle changes evident within 3 hrs
• in MRI (not done often) appears hyper-intense within hours of onset

Answer 146

A

- maximise reversible ischaemic tissue 
• ensure hydration
• keep O2 sats > 95%
- thrombolysis
- if time of onset is unknown and thus thrombolysis is unsuitable then give aspirin daily for 2 weeks then lifelong clopidogrel

Answer 147

A

can be given up to 4.5 hrs post-onset of symptoms
must CT head/MRI first to rule out haemorrhage, otherwise will make it worse and cause death
give tissue plasminogen activator e.g. IV alteplase
then start antiplatelet therapy 24hrs after thrombolysis

Answer 148

A

recent surgery in last 3 months
recent arterial puncture
history of active malignancy
evidence of brain aneurysm
patient on anticoagulation
severe liver disease (abnormal clotting)
acute pancreatitis
clotting disorder

Answer 149

A

frequent GCS monitoring
antiplatelets contraindicated
any anticoagulants should be reversed and for warfarin reversal use beriplex and vitamin K
control hypertension
manual decompression of raised ICP, can also reduce ICP by giving diuretic e.g. mannitol
surgery may be required

Answer 150

A

platelet treatment (lifelong if already had stroke)
cholesterol-lowering treatment
atrial fibrillation treatment e.g. warfarin or new oral anticoagulants e.g. apixaban
blood pressure treatment

Answer 151

A

4.5 hour time frame for thrombolysis (alteplase) as long as CT head confirms it’s ischaemic and that there are no contraindications

Answer 152

A

spontaneous bleeding into the subarachnoid space between the arachnoid and the pia mater
can often be catastrophic
typical age 35-65
account for 5% of strokes
most common cause is rupture of Berry aneurysm

Answer 153

A

rupture of saccular aneurysms (80%) e.g. Berry aneurysms; associated with PCKD and coarctation of aorta
atriovenous malformation (10%)
no cause found (15%)
rare (bleeding disorders, mycotic aneurysms, acute bacterial meningitis, tumours)

Answer 154

A

appear as a round outpouching; most common form of cerebral aneurysm
• rupture of the junction of the posterior communicating artery with the internal carotid or of the anterior communicating artery with the anterior cerebral artery in the circle of Willis
• 15% are multiple i.e. multiple aneurysms

Answer 155

A

vascular developmental malformation often with a fistula between arterial and venous systems causing high flow through the AVM and high-pressure arterialisation of draining veins

Answer 156

A

hypertension
known aneurysm
family history
disease that predispose to aneurysm
smoking
bleeding disorders
post-menopausal decreased oestrogen

Answer 157

A

polycystic kidney disease
Ehlers-Danlos syndrome
coarctation of aorta

Answer 158

A

most common cause is ruptured aneurysm which leads to tissue ischaemia (since less blood can reach tissue) and rapid raised ICP as the fast flowing arterial blood acts like a space-occupying lesion, puts pressure on the brain and results in deficits if not resolved quickly

Answer 159

A

sudden onset severe occipital thunder clap headache, like being kicked in the head, severe pain
vomiting, collapse, seizures and coma often follow
depressed level of consciousness
coma/drowsiness may last for days
neck stiffness
Kernig’s sign (unable to extend patients leg at the knee when the thigh is flexed)
Brudzinski’s sign (when patients neck is flexed by doctor, patient will flex their hips and knees)
retinal and vitreous bleeds
papilloedema - dilated optic disc
vision loss or diplopia (double vision)
marked increase in BP as a reflex to following haemorrhage
focal neurology at presentation may suggest site of aneurysm
sentinel headache

Answer 160

A

unable to extend patients leg at the knee when the thigh is flexed
seen in subarachnoid haemorrhage

Answer 161

A

when patients neck is flexed by doctor, patient will flex their hips and knees
seen in subarachnoid haemorrhage

Answer 162

A

a headache that resolves by itself and no other symptoms are present
presumed to result from a small leak from an aneurysm

Answer 163

A

must be differentiated from migraine (short time taken to reach maximal intensity and neck stiffness indicates SAH)
in primary care only 25% of those with severe, sudden ‘thunderclap’ headache actually have a SAH
in 50-60%, no cause is found for headache
meningitis
intracerebral bleeds
cortical vein thrombosis

Answer 164

A

ABG (to exclude hypoxia)
head CT
CT angiography
lumbar puncture

Answer 165

A

detects >90% of SAH within 1st 48hrs

* seen as a ‘star shaped lesion’ due to blood filling in gyro patterns around the brain and ventricles

Answer 166

A

done if CT normal but SAH still suspected
CSF in SAH is uniformly bloody early on and becomes xanthochromic after several hours due to breakdown products of Hb (bilirubin)
xanthochromia presence confirms SAH

Answer 167

A

refer all proved SAH to neurosurgeons immediately
maintain cerebral perfusion by keeping well hydrated (IV fluids) and aim for BP <160mmHg
administer Ca2+ blocker to reduce vasospasm and consequent morbidity from cerebral ischaemia e.g. IV/oral nimodipine
endovascular coiling
surgery; intracranial stents and balloon remodelling for wide-necked aneurysms

Answer 168

A

preferred to surgical clipping since has lower complication rate where possible
promotes thrombosis and ablation of aneurysm
first line treatment where angiography shows aneurysm

Answer 169

A

rebleeding
cerebral ischaemia due to vasospasm can result in permanent deficit
hydrocephalus due to blockage of arachnoid granulations requires ventricular or lumbar drain
hyponatraemia

Answer 170

A

caused by the accumulation of blood in the subdural space between the arachnoid and dura mater following rupture of a bridging vein between cortex and venous sinus (vulnerable to deceleration injury)
considered very treatable in all those whose conscious level fluctuates and also in those having an ‘evolving stroke’, especially if on anticoagulants

Answer 171

A

most common where patient has a small brain e.g. alcoholics or dementia, babies that have suffered trauma or elderly that have brain atrophy (makes the bridging veins more vulnerable)
majority of SDH’s are from trauma but the trauma is often forgotten as it was minor or long ago (up to 9 months)
chronic, apparently spontaneous SDH is common in elderly and also occurs with anticoagulants

Answer 172

A

trauma either due to deceleration due to violent injury or due to dural metastases results in bleeding from bridging veins between the cortex and
venous sinuses
bridging veins bleed and form a haematoma between the dura and arachnoid which reduces pressure and stops bleeding
days/weeks later, the haematoma autolyses due to the massive increase in oncotic and osmotic pressure, thus water is sucked into the haematoma resulting in the haematoma enlarging
this results in a gradual rise in intra-cranial pressure (ICP) over many weeks
shifting midline structures away from the side of the clot and if untreated leads to eventual tectorial herniation and coning (brain herniates through foramen magnum - causes significant damage)

Answer 173

A

traumatic head injury, cerebral atrophy/increasing age - makes bridging veins more vulnerable
alcoholism (caused cerebral atrophy), anticoagulation and physical abuse of infant

Answer 174

A

interval between injury and symptoms can be days to weeks or months
fluctuating level of consciousness (35%) and/or insidious physical or intellectual slowing
sleepiness
headache
personality change
unsteadiness
signs of raised ICP e.g. headache, vomiting, nausea, seizure and raised BP
focal neurology e.g. hemiparesis or sensory loss: occurs late and often long after injury, mean time is 63 days
seizures occasionally
stupor, coma and coning may follow

Answer 175

A

due to decrease in brain weight and increase in subdural space with increasing age, a haematoma and its symptoms develop much slower as brain has more compliance to raised ICP

Answer 176

A

stroke
dementia
CNS masses e.g. tumours or abscess
SAH
extradural haemorrhage

Answer 177

A

CT head

- MRI head for subacute haematomas and smaller haematomas

Answer 178

A

• diffuse spreading, hyperdense crescent shaped
collection of blood over 1 hemisphere
• as the clot ages and protein degradation occurs it becomes isodense (same colour as brain tissue) and eventually becomes hypodense
• shifting of midline structures seen

Answer 179

A

sickle/crescent shape differentiates subdural haemorrhage from extradural haemorrhage

Answer 180

A

assess and manage ABCs, prioritise head CT
stabilise patient
refer to neurosurgeons: irrigation/evacuation via burr twist drill and burr hole craniotomy
address cause of trauma
IV mannitol to reduce ICP

Answer 181

A

suspect this if after head injury, conscious level falls or is slow to improve or there is a lucid interval
collection of blood between the dura mater and the bone usually caused by head injury
most commonly due to a traumatic head injury to the temple resulting in fracture of the temporal or parietal bone causing laceration of the middle meningeal artery

Answer 182

A

usually occurs in young adults (rare <2 and >60)

Answer 183

A

whilst haematoma is still small and there is still some bleeding
doesn’t really bother you physically
can last several hours or even days
followed by altered consciousness

Answer 184

A

severe headache, nausea and vomiting, confusion and seizures due to rising ICP and/or hemiparesis with brisk reflexes
rapid rise in ICP as the epidural space is full of blood resulting in brain compression
ipsilateral pupil dilates, coma deepens, bilateral limb weakness develops and breathing becomes deep and irregular (signs of brainstem compression)
decreased GCS
coning: brain herniates through the foramen magnum
death due to respiratory arrest if surgical intervention not done fast enough
bradycardia and raised BP are late signs

Answer 185

A

epilepsy, carotid dissection and carbon monoxide poisoning (fit with lucid period)
subdural haematoma, subarachnoid haemorrhage, meningitis

Answer 186

A

CT head

- skull X-ray

Answer 187

A

gold standard

* shows hyperdense haematoma that is biconvex/lenseshaped/lemon shaped and adjacent to the skull

Answer 188

A

may be normal or show fracture lines crossing the course of the middle meningeal artery
skull fracture increases extradural haemorrhage risk, so do urgent CT for anyone with suspected fracture

Answer 189

A

ABCDE emergency management; assess and stabilise patient
give IV mannitol if increased ICP
refer to neurosurgery for clot evacuation and/or ligation of bleeding vessel
maintain airway via intubation and ventilation in unconscious patient

Answer 190

A

the recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting in seizures
epilepsy is an ongoing liability to recurrent epileptic seizures
chronic disorder; need at least 2 seizures to be defined as epileptic

Answer 191

A

paroxysmal/unprovoked event in which changes of behaviour, sensation or cognitive processes are caused by excessive, hypersynchronous neuronal discharges in the brain

Answer 192

A

motor signs of electrical discharges
many of us would have seizures in abnormal metabolic circumstances e.g. low Na+ or hypoxia (reflex anoxic seizures in faints)
we would not normally be said to have epilepsy

Answer 193

A

common
incidence is age-dependent, it is highest at the extremes of life with most cases starting before 20 or after 60
can often go into remission
seizures usually last 30-120 seconds

Answer 194

A

2/3rds are idiopathic often familial
cortical scarring (head injury, cerebrovascular disease, CNS infection)
space-occupying lesion
stroke
tuberous sclerosis
Alzheimer’s or dementia
alcohol withdrawal

Answer 195

A

family history
premature born babies who are small for their age
abnormal blood vessels in brain
Alzheimer’s or dementia
use of drugs
stroke/brain tumour/infection

Answer 196

A

lasting hours or days may rarely precede the seizure

- not part of the seizure, results in change of mood or behaviour

Answer 197

A

part of seizure where the patient is aware
strange feeling in the gut, deja-vu or strange smells or flashing lights
implies a partial (focal) seizure often but not necessarily from the temporal lobe

Answer 198

A

headache, confusion, myalgia and a sore tongue
temporary weakness after a focal seizure in motor cortex (Todd’s palsy)
dysphasia following a focal seizure in the temporal lobe

Answer 199

A

primary generalised (40%) and partial/focal (57%) seizures

Answer 200

A

simultaneous onset of electrical discharge throughout whole cortex (involving both hemispheres), with no localising features referable to only one hemisphere
bilateral symmetrical and synchronous motor manifestations
always associated with loss of consciousness or awareness

Answer 201

A

focal onset, with features referable to a part of one hemisphere
often seen with underlying structural disease
electrical discharge is restricted to a limited part
of the cortex of one cerebral hemisphere
these may later become generalised (e.g. secondarily generalised tonic-clonic seizures)

Answer 202

A

generalised tonic-clonic seizure (grand-mal)
typical absence seizure (petit mal)
myoclonic seizure
atonic (akinetic seizure)

Answer 203

A

often no aura
tonic phase: rigid, stiff limbs; person will fall if standing
clonic phase: generalised, bilateral, rhythmic muscles jerking, lasting for seconds to minutes
loss of consciousness
eyes remain open and tongue often bitten
there may be incontinence of urine/faeces
followed by a period of drowsiness, confusion or coma for several hours post-ictally

Answer 204

A

usually a disorder of childhood
child ceases activity, stares and pales for a few seconds only
often do not realise that they’ve had an attack
on EEG characterised by a 3-Hz spike and wave activity
children with petit-mal tend to develop generalised tonic-clonic seizures in adult life

Answer 205

A

sudden isolated jerk of a limb, face or trunk

- patient may be thrown suddenly to the ground, or have a violently disobedient limb

Answer 206

A

sudden sustained increased tone with a characteristic cry/grunt
intense stiffening of body (tonic)
stiffening not following by jerking

Answer 207

A

sudden loss of muscle tone and cessation of movement resulting in a fall

Answer 208

A

simple partial seizure
complex partial seizure
partial seizure with secondary generalisation

Answer 209

A

not affecting consciousness or memory
awareness is unimpaired with focal motor, sensory (olfactory, visual etc.), autonomic or psychic symptoms
no post-ictal symptoms

Answer 210

A

affecting awareness or memory before, during or immediately after the seizure
most commonly arise from the temporal lobe
post-ictal confusion is common with seizures arising from the temporal lobe, whereas recovery is rapid after seizures in the frontal lobe

Answer 211

A

in 2/3rds of patients with partial seizures, the electrical
disturbance, which starts focally (as either a simple or complex partial seizure), spreads widely causing a secondary generalised seizure which is typically convulsive

Answer 212

A

aura (80%): deja-vu, auditory hallucinations, funny smells, fear
anxiety or out of body experience, automatisms e.g. lip smacking, chewing, fiddling

Answer 213

A

motor features such as posturing or peddling movements of the leg
Jacksonian march; seizure “marches” up or down the motor homunculus starting in face or thumb
post-ictal Todd’s palsy

Answer 214

A

sensory disturbances e.g. tingling/numbness

Answer 215

A

visual phenomena e.g. spots, lines or flashes

Answer 216

A

epilepsy: tongue biting, head turning, muscle pain, loss of consciousness, cyanosis, post-ictal symptoms
syncope is the loss of consciousness due to hypoperfusion to brain: caused by prolonged upright position, sweat prior to loss of consciousness, nausea, pre-syncopal symptoms

Answer 217

A

non-epileptic seizures are situational
non-epileptic is longer, closed mouth/eyes during tonic-clonic movements, pelvic thrusting, do not result from sleep, no incontinence or tongue biting
there are pre-ictal anxiety symptoms in non-epileptic seizure

Answer 218

A

postural syncope, cardiac arrhythmia, TIA, migraine, hyperventilation, hypoglycaemia, panic attacks or non-epileptic seizure

Answer 219

A

EEG
MRI (imaging of the hippocampus is used)
CT head (used in emergency to look for space-occupying lesion and identify/exclude structural abnormalities)
blood tests
genetic testing e.g. in juvenile myoclonic epilepsy

Answer 220

A

not diagnostic
performed to support diagnosis of epilepsy when history suggests it
may help determine seizure type and what epilepsy syndrome it is
frequently it is normal between attacks and false-positive may be detected in non-epileptics
typically a 3Hz spike and wave is seen in a absence seizure of the temporal lobe

Answer 221

A

FBC, electrolytes, Ca2+, renal function, liver function, urine biochemistry and blood glucose levels
done to rule out metabolic causes and discover comorbidities

Answer 222

A

ensure patient harms themselves as little as possible (ABCDE)
check glucose
prolonged seizure (longer than 3 minutes) or repeated seizures are treated with rectal/IV diazepam or lorazepam; repeat twice
IV phenytoin loading
if still fitting then anaesthetist involvement for anaesthetics and ventilation

Answer 223

A

make sure it’s not syncope or non-epileptic seizure and decide whether it is partial or generalised seizures

Answer 224

A

generally drugs are not advised after just one fit unless the risk of recurrence is high e.g structural brain lesion or focal CNS deficit
epilepsy is resistant to drug treatment in a 1/3rd of patients

Answer 225

A

oral sodium volproate (weight gain, liver failure, teratogenic)
oral lamotrigine (maculopapular rash, blurred vision, vomiting)
oral carbamazepine (diplopia, rashes, leucopenia, impaired balance, drowsiness)

Answer 226

A

oral sodium valproate
oral lamotrigine
oral ethosuximide (rashes, night tremors)

Answer 227

A

carbamazepine (first line)
sodium valproate
lamotrigine

Answer 228

A

used if drugs are not working
if a single defined cause if identified such as hippocampal sclerosis or low grade tumour then surgical resection can offer 70% chance of seizure freedom
alternative is vagal nerve stimulation which can reduce seizure frequency and severity in 33%

Answer 229

A

medical emergency
continuous seizures without recovery of consciousness
when grand-mal seizures follow one another, there is a risk of death from cardiorespiratory failure
caused by stopping anti-epileptic treatment, alcohol abuse

Answer 230

A

avoid swimming alone, avoid dangerous sports e.g. rock climbing, leave door open when taking bath, cannot drive sometimes

Answer 231

A

sudden unexpected death epilepsy

more common in uncontrolled epilepsy
can be related to nocturnal seizure-associated apnoea or asystole

Answer 232

A

a syndrome caused by a number of brain disorders which causes memory loss, difficulties with thinking, problem-solving or language as well as difficulties with activities of daily living

Answer 233

A

rare under 55 yrs
prevalence rises with age
AD is more common in females than males
vascular and mixed dementias are more common in males than females

Answer 234

A

Alzheimer’s disease (50%)
vascular dementia (25%)
Lewy-body dementia (15%)
fronto-temporal (Pick’s) dementia
Huntington’s
liver failure
HIV
prion diseases e.g. Creutzfeldt-Jakob
vitamin B12/folate deficiency

Answer 235

A

most common cause
degeneration of the cerebral cortex, with cortical atrophy
accumulation of beta-amyloid peptide, a degradation product of amyloid precursor protein, results in progressive neuronal damage, neurofibrillary tangles, increases in the number of amyloid plaques and the loss of ACh

Answer 236

A

brain damage due to cerebrovascular disease; either major stroke, multiple smaller unrecognised strokes or chronic changes in smaller vessels
presents with signs of vascular pathology e.g. raised BP, past strokes and focal CNS signs

Answer 237

A

3rd most common cause of dementia
deposition of abnormal protein within neurons in the brain stem and neocortex
presents with fluctuating cognitive impairment, detailed visual hallucinations
associated with Parkinsons

Answer 238

A

specific degeneration/atrophy of the frontal and temporal lobes of the brain
behavioural and personality change, early preservation of episodic memory and spatial orientation, emotional unconcern, lowers inhibitions
mixed dementia
Parkinson’s dementia

Answer 239

A

family history
age
Down’s syndrome
alcohol use
obesity
high BP
hypercholesterolaemia
diabetes
atherosclerosis
depression
high oestrogen levels

Answer 240

A

insidious onset with steady progression over years
short-term memory loss is usually the most prominent early symptom, but subsequently there is slow disintegration of the personality and intellect, eventually affecting all aspects of cortical function
decline in language (difficulty naming and in understanding what is being said), visuospatial skills, apraxia (impaired ability to carry out skilled motor tasks and agnosia (failure to recognise objects e.g. clothing, people and places)

Answer 241

A

stepwise deterioration with decline followed by short periods of stability
history of TIAs and/or strokes
evidence of atheropathy

Answer 242

A

fluctuating cognition with pronounced variation in attention and alertness
prominent or persistent memory loss may not occur in the early stages
impairment in attention, frontal, subcortical and visuospatial ability is often prominent
depression and sleep disorders occur
visual hallucinations
Parkinsons is common
loss of inhibitions

Answer 243

A

substance abuse, hypothyroidism, space-occupying intracranial lesions, Huntington’s

Answer 244

A

history; assess cognitive functions by asking various questions
MMSE used to screen for cognitive function
exclude rare treatable causes of dementia (substance abuse, vitamin B12 deficiency, hypothyroidism)
blood tests
neuropsychology
brain CT in younger patients or those with atypical presentation
MRI to see extent of atrophy
assess brain function (PET, SPECT, functional MRI)

Answer 245

A

score of 25+ out of 30 is normal, 18-24 = mild/moderate impairment and a score of 17 or below indicates serious impairment

Answer 246

A

healthy behaviours
smoking cessation, good diet, physical activity and low alcohol
engaging in more than 6 leisure activities lowers risk
education, occupation, premorbid IQ and mental activities decreases risk
changes in CSF amyloid-beta (Alzheimer’s) are seen 25yrs before onset of symptoms

Answer 247

A

ACE inhibitor in alzheimer’s to increase ACh e.g. oral donepezil or oral rivastigmine
blood pressure control to reduce further vascular damage, particularly in vascular dementia such as ACE-inhibitors

Answer 248

A

degenerative movement disorder caused by a reduction in dopamine in the substantia nigra

Answer 249

A

increasing prevalence with age
peak age of onset is 55-65 yrs
more common in males than females

Answer 250

A

idiopathic
drug induced
combination of: environmental factors, Parkinson’s genes, oxidative stress and mitochondrial dysfunction
• environmental factors: pesticides, methyl-phenyl tetrahydropyridine found in illegal opiates
• mutation in parkin gene and alpha-synuclein gene
• oxidative stress and mitochondrial dysfunction

Answer 251

A

male
increasing age
family history
being a non-smoker increases risk of parkinsons

Answer 252

A

this results in the progressive degeneration of dopaminergic neurons from the pars compacta of the substantia nigra in the midbrain that projects to
the striatum (caudate and putamen) of the basal ganglia
- loss of dopaminergic neurons leads to reduced striatal dopamine levels, leading to inhibition of the thalamus leading to decreased movement and symptoms of Parkinsons
- the extent of nigostriatal dopaminergic cell loss correlates with the degree of akinesia (muscle rigidity, stiffness and lack of responsiveness)

Answer 253

A

contain tangles of alpha synuclein and ubiquitin
become gradually more widespread as the condition progresses, spreading from the lower brainstem to the midbrain then into the cortex

Answer 254

A

onset of symptoms is gradual and commonly presents with impaired dexterity or unilateral foot drop
asymmetrical; one side always worse than the other

Answer 255

A

anosmia - reduced sense of smell
depression/anxiety
aches and pains
REM sleep disorders
urinary urgency
hypotension and constipation

Answer 256

A

tremor
rigidity (since it’s an extrapyramidal lesion)
bradykinesia/hypokinesia

Answer 257

A

worse at rest and often asymmetrical
usually most obvious in the hands (pill-rolling of the thumb and fingers)
improved by voluntary movements and made worse by anxiety
4-6 cycles/sec (slower than cerebellar tremor)
only in Parkinson’s will you see issue with repetitive hand movements with worsening in rhythm the longer attempted

Answer 258

A

occurs because Parkinson’s is an extrapyramidal lesion
increased tone in the limbs and trunk
limbs resists passive extension throughout movement (lead-pipe rigidity or cogwheel when combined with tremor)
this is opposed to the hypertonia of a UMN lesion, which is spasticity where resistance falls away as the movement continues (clasp-knife)
increased tone and thus rigidity over entire radius of joint movement
can cause pain and problems with turning in bed

Answer 259

A

- slow to initiate movement and slow, low-amplitude excursions in repetitive actions
• reduced blink rate
• monotonous hypophonic speech
• micrographia (writing smaller)
- gait
- expressionless face (hypomimesis)

Answer 260

A

asymmetrical, reduced arm swing
narrow gait
stooped posture and small shuffling steps
festinance: shuffling steps, maybe dragging foot with flexed trunk
difficulty initiating movement and turning
poor balance

Answer 261

A

onset of symptoms is gradual and commonly presents with impaired dexterity or unilateral foot drop
onset is asymmetrical
before motor symptoms develop
classic triad (tremor, rigidity, bradykinesia/hypokinesia)
difficulty with fine movements e.g. problems doing up buttons
Parkinsonian gait
speech becomes quiet, indistinct and flat
drooling of saliva and swallowing difficulty is a late feature (can lead to aspiration pneumonia as a terminal event)
depression is common
constipation is common
increased urinary frequency

Answer 262

A

benign essential tremor (more common); worse on movement and rare whilst at rest
multiple cerebral infarcts, Lewy body dementia, drug-induced, Wilson’s disease, trauma and dopamine antagonists

Answer 263

A

treat with beta-blockers e.g. propanolol (contraindicated with asthma/diabetes)
primidone (anti-seizure) or gabapentin (anti-epileptic)

Answer 264

A

diagnosis is based on history and examination
can confirm by response to levodopa
MRI head (can show atrophy, used to exclude tumours or normal pressure hydrocephalus)
dementia, incontinence, symmetry and early falls suggest that it’s not Parkinsons

Answer 265

A

the gold standard treatment is oral levodopa given alongside a decarboxylase inhibitor e.g. co-careldopa or co-beneldopa
dopamine agonists e.g. oral ropinirole or oral pramiprexole
monoamine oxidase B inhibitors e.g. oral selegiline or oral rasagiline
catechol-O-methyltransferase inhibiors e.g. oral entacapone or oral tolcapone
deep brain stimulation may help those who are partly-dopamine responsive
surgical ablation of overactive basal ganglia circuits

Answer 266

A

explain that the disease is slowly progressive and although incurable it’s amenable to palliation
balance problems, speech and gait disturbance do not respond to medication thus physiotherapy is the mainstay treatment for these
physical activity is beneficial and should be encouraged

Answer 267

A

oral levodopa given alonside a decarboxylase inhibitor e.g. co-careldopa or co-beneldopa

Answer 268

A

levodopa (L-dopa) is a precursor to dopamine, but dopamine cannot cross the blood brain barrier whereas L-dopa can
a decarboxylase inhibitor is given with it, prevents peripheral conversion of L-dopa to dopamine and therefore reduces the peripheral side effects as well as maximising the dose that crosses the BBB
once crossed, the L-dopa can be taken up by dopaminergic neurones and converted into dopamine and used

Answer 269

A

nausea, vomiting, arrhythmias, psychosis and visual hallucinations
reduced efficacy over time even if dose is increased
• effect can wear off in 5-10yrs and won’t work for as long as before; L-dopa is usually avoided until very late or if symptoms have worsened
the use of dopamine antagonists, MAO-B and COMT inhibitors can allow the delay in starting L-dopa
on-dyskinesias
off-dyskinesias
freezing (unpredictable loss of mobility)

Answer 270

A

hyperkinetic, choreiform movement whenever drugs work - repetitive, rapid, jerky well-coordinated involuntary movements (seen in Huntington’s)

Answer 271

A

fixed, painful dystonic posturing (twisting and repetitive movements or abnormal fixed postures - caused by sustained repetitive muscle contractions)

Answer 272

A

co-careldopa or co-beneldopa

Answer 273

A

oral ropinorole or oral pramiprexole

Answer 274

A

side effects: drowsiness, nausea, hallucinations, compulsive behaviour
avoid bromocriptine/cabergoline as they can cause cardiac valvulopathy

Answer 275

A

oral selegiline or oral rasagiline

Answer 276

A

these inhibit MAO-B enzymes which breakdown dopamine, thus they result in a reduction of dopamine breakdown so dopamine remains for longer
used to delay starting L-Dopa and to reduce the wearing off of L-Dopa
side effects: postural hypotension and AF

Answer 277

A

oral entacapone or oral tolcapone

Answer 278

A

inhibit COMT, which breaks down dopamine

- tolcapone can cause liver damage

Answer 279

A

neuropsychiatric complications e.g. depression, dementia and psychosis are common and reflect disease progression or drug side-effects
SSRIs and anti-psychotics can be used

Answer 280

A

deep brain stimulation may help those who are partly-dopamine responsive
surgical ablation of overactive basal ganglia circuits e.g. subthalamic nuclei

Answer 281

A

Huntington’s is a cause of chorea and is a neurodegenerative disorder characterised by the lack of the inhibitory neurotransmitter GABA

Answer 282

A

relentlessly progressive, jerky, explosive, semi-purposeful movements, rigidity, involuntary movements flitting from one part of the body to another; continuous flow
can’t sit still
may begin as general restlessness, unintentionally initiated movements and lack of coordination
stops when sleeping

Answer 283

A

autosomal dominant condition with full penetrance; all gene carriers will develop disease
incurable, progressive neurodegenerative disorder
presents in middle age initially with a prodromal phase of mild symptoms e.g. irritability, depression and incoordination then progressing to psychiatric
and cognitive symptoms
very rare, prevalence worldwide is 5 per 100000

Answer 284

A

mutation on chromosome 4 resulting in the repeated expression of CAG sequence

Answer 285

A

family history

- having a parent with Huntington’s; child has 50% risk of getting it

Answer 286

A

repeated expression of CAG sequence leads to the translation of an expanded polyglutamine repeat sequence in the Huntington gene, the protein gene product the function is expansion is thought to be a toxic ‘gain-of-function mutation’
progressive cerebral atrophy with marked loss of neurones in the caudate nucleus and putamen of the basal ganglia; there is specifically loss of the corpus striatum GABA-nergic and cholinergic neurons
this results in decreased ACh and GABA synthesis in the striatum
GABA is the main inhibitory neurotransmitter, loss of this will result in decreased inhibition of dopamine release and therefore result in excessive thalamic stimulation and thus excessive movements (chorea)

Answer 287

A

the more CAG repeats present, the earlier the symptom onset:
• most adult onset have 36-55 repeats
• early onset i.e. from childhood have over 60 repeats

Answer 288

A

often prodromal phase of mild psychotic and behavioural symptoms, then chorea develops
dysarthria (unclear speech), dysphagia and abnormal eye movements (behavioural change, depression/anxiety)
psychiatric problems
dementia
associated with seizures
eventually occurs until death; death usually occurs within 15yrs of diagnosis, usually from an intercurrent illness e.g. infection

Answer 289

A

Huntington’s is the commonest cause of chorea
other causes or chorea:
• Sydenham’s chorea (Rheumatic fever)
• Creutzfeldt-Jakob Disease (prion)
• Wilson’s disease
• SLE
• stroke of basal ganglia

Answer 290

A

diagnosis is mainly clinical
genetic testing, shows many CAG repeats
CT/MRI

Answer 291

A

shows caudate nucleus atrophy and increased size of the frontal horns of the lateral ventricles (signs of brain matter destruction)
imaging is not useful early on in disease process

Answer 292

A

there is no treatment to prevent progression
counselling to patient and family, genetic counselling to any children of patients
symptomatic management of chorea: benzodiazepines, sulpiride (neuroleptic, depresses nerve function), tetrabenzine (dopamine depleting)
antidepressants such as SSRIs
antipsychotic medication such as neuroleptics e.g. haloperidol
to treat aggression use risperidone

Answer 293

A

no underlying cause relevant to the headache

* examples include; migraine (20% of population), cluster and tension headache (affect 99% in lifetime)

Answer 294

A

there is an underlying cause

- e.g. meningitis, SAH, giant cell arteritis, medication overuse headache

Answer 295

A

HIV or immunosuppressed
fever
thunderclap headache (SAH)
seizure and new headache
suspected meningitis
suspected encephalitis
red eye? acute glaucoma
headache + new focal neurology e.g. papilloedema

Answer 296

A

trigeminal neuralgia; a painful cranial neuropathy

Answer 297

A

recurrent throbbing headache often preceded by an aura and associated with nausea, vomiting and visual changes
a migraine aura may affect the patients eyesight with visual phenomena such as fortification spectra (zig-zag lines), shimmering or scotomas, but may also result in pins and needles, dysphasia and rarely weakness of limbs and motor function

Answer 298

A

most common cause of episodic headache (recurrent)
more common in females than males
in 90% onset if before 40yrs
if onset >50 then pathology should be sought
usually the severity of migraine decreases with advancing age

Answer 299

A

CHOCOLATE:

Chocolate
Hangovers
Orgasms
Cheese
Oral contraceptives
Lie-ins
Alcohol
Tumult - loud noise
Exercise

Answer 300

A

CHOCOLATE (partial triggers)
brain chemical imbalance may be cause
may be caused by changes in the brainstem and its interactions with the trigeminal nerve

Answer 301

A

family history
female
age; can occur at any age but majority have first migraine in adolescence

Answer 302

A

genetic and environmental factors play a role
genetic factors play a role in causing neuronal-hyper-excitability
changes in brainstem blood flow lead to an unstable trigeminal nerve nucleus and nuclei in the basal thalamus
cortical spreading depression; self-propagating wave of neuronal and glial depolarisation that spreads across the cerebral cortex is thought to cause the aura of migraine and leads to the release of inflammatory mediators which impact on the trigeminal nerve nucleus
this results in release of vasoactive neuropeptides including calcitonin-gene-related peptide and substance P; this results in neurogenic inflammation, vasodilation and plasma protein extravasation, leading to pain that propagates all over the cerebral cortex

Answer 303

A

there may be a prodrome that precedes the headache by hours/days (e.g. yawning, cravings, mood/sleep changes)
migraine without aura
symptoms during headache
not attributable to another disorder

Answer 304

A

attacks last 4-72 hours
two of the following: unilateral, pulsing, moderade/severe pain in head, aggravated by routine physical actvity
during headache at least one of: nausea and/or vomiting during headache, photophobia, sound sensitivity
not attributable to another disorder

Answer 305

A

at least 2 attacks
aura precedes the attack by minutes and may persist during it
unilateral, pulsatile headache
chaotic cascading, jumbling, distorting lines, dots or zigzags
scotoma (black hole in visual field)
hemianopia
paraesthesiae spreading from fingers to face

Answer 306

A

unilateral pain
throbbing-type pain
moderate to severe intensity
motion sensitivity (headache made worse with head movement of physical activity)

Answer 307

A

nausea/vomiting
photophobia/phonophobia
normal examination with no other attributable cause

Answer 308

A

tension headache (bilateral, tight-band around head), cluster headache (excruciating, autonomic symptoms), medication over-use headache
sudden migraine may resemble meningitis or subarachnoid haemorrhage
the visual and hemisensory symptoms must be distinguished from thromboembolic TIAs (in TIAs the maximum deficit is present immediately and headache is unusual)
brain tumour (rare cause of headaches) and temporal arteritis

Answer 309

A

mainly clinical diagnosis
always examine eyes, BP, head and neck
exclude other causes

Answer 310

A

lab tests (CRP and ESR)
indications for neuroimaging (CT/MRI)
lumbar puncture

Answer 311

A

worst/severe headache; thunderclap headache
change in pattern of migraine
abnormal neurological exam
onset > 50 yrs
epilepsy
posteriorly located headache

Answer 312

A

worst headache of life; thunderclap headache
severe rapid onset headache, progressive headaches, unresponsive headaches
neuroimaging should precede lumbar puncture to rule out mass/lesion/raised ICP

Answer 313

A

do not offer ergots e.g. ergotamine or opioids
triptans e.g. sumatriptan
NSAIDs e.g. ketoprofen, naproxen or aspirin (avoid paracetamol or ibuprofen)
and/or anti-emetic e.g. prochlorperazine

Answer 314

A

e.g. sumatriptan
selectively stimulate 5-hydroxytryptamine receptors in brain
contraindicated in ischaemic heart disease, coronary spasm and uncontrolled high BP
side effects: arrhythmias, angina, MI

Answer 315

A

reduce triggers
if more than 2 attacks a month, or acute treatment required more than twice a week
beta blockers
tricyclic anti-depressant; side effects: drowsiness, dry mouth and reduced vision
anti-convulsant e.g. topiramate; side effects: reduced memory

Answer 316

A

most common type of primary headache
pain can radiate from lower back of the head, the neck, eyes or other muscle groups in the body, typically affecting both sides of the head
most chronic daily and recurrent headaches are tension headaches

Answer 317

A

the commonest primary headache
can be episodic (<15 days/month) or chronic (>15 days a month for at least 3 months)
no organic cause

Answer 318

A

stress
sleep deprivation
bad posture
hunger
eyestrain
anxiety
noise

Answer 319

A

episodic (<15 days/month) or chronic (>15 days a month for at least 3 months)
usually has one of the following: bilateral, pressing/tight non-pulsatile, mild/moderate intensity, scalp muscle tenderness
without vomiting or sensitivity to head movement, no aura
not aggravated by physical activity
tight band-like sensation
pressure behind eyes, mild-moderate pain
headaches can last from 30 mins to 7 days
not attributed to other disorder

Answer 320

A

migraine, cluster headache, giant cell arteritis, drug-induced headache

Answer 321

A

clinical diagnosis from history

Answer 322

A

reassurance and lifestyle advice,avoidance of triggers
stress relief e.g massage or acupuncture
symptomatic treatment for episodes occurring >2 days a week

Answer 323

A

aspirin
paracetamol
NSAIDs e.g. ibuprofen
no opioids
limit the use of analgesia to no more than 6 days a month to reduce chance of medication-overuse headache
consider tricyclic antidepressants e.g. amitriptyline

Answer 324

A

worsens whilst on regular analgesia, especially on opioids
other causes are mixed analgesics e.g. paracetamol and codeine/opiates, ergotamine and triptans
common reason for episodic headache becoming chronic daily headache

Answer 325

A

neurological disorder characterised by recurrent severe headaches on one side of the head, typically around the eye
most disabling primary headache

Answer 326

A

distinct from migraine
much rarer than migraine; 1 per 1000
more common in males than females
affects adults, typically between 20-40 yrs
commoner in smokers

Answer 327

A

smoker
male
autosomal dominant gene plays a role

Answer 328

A

unknown
may be due to superficial temporary artery smooth muscle hyper-reactivity to serotonin
there are hypothalamic grey matter abnormalities too
autosomal dominant gene has a role too

Answer 329

A

abrupt onset
rapid onset of excrutiating pain around one eye, temple or forehead
ipsilateral cranial autonomic features
pain is strictly unilateral and almost always affects the same side
rises to crescendo over minutes and lasts 15-160mins, once or twice a day; usually at the same time
often nocturnal/early morning - often wakes patient from sleep
vomiting
episodic; clusters last 4-12 weeks and are followed by pain-free periods of months or even 1-2 yrs before the next cluster
can be chronic (attacks for more than 1yr without remission) instead of episodic

Answer 330

A

eye may become watery and bloodshot with lid swelling, lacrimation,
facial flushing
rhinorrhea (blocked nose)
miosis (excessive pupil constriction) +/- ptosis (drooping or falling of upper eyelid), seen in 20% of attacks

Answer 331

A

clinical diagnosis

- at least 5 headache attacks fulfilling the clinical presentation criteria

Answer 332

A

calcium channel blocker is first line prophylaxis
avoid alcohol during cluster period
corticosteroids may help during cluster
analgesics are unhelpful
100% 15L O2 for 15mins via a non-rebreathable mask (not if COPD)
triptan e.g. SC sumatriptan

Answer 333

A

a chronic, debilitating condition affecting the trigeminal nerve, resulting in intense and extreme episodes of pain

Answer 334

A

peak incidence between 50-60yrs
more common in females than males
prevalence increases with age
may be due to a genetic disposition
almost always unilateral

Answer 335

A

in most cases it is due to compression of the trigeminal nerve by a loop of vein or artery
can be due to local pathology such as aneurysms, meningeal inflammation, tumours; local pathology is more common in younger people as a cause of compression
a fifth nerve lesion is due to pathology
hypertension is the main risk factor
triggers: washing affected area, shaving, eating, talking and dental prostheses

Answer 336

A

within the brainstem - tumour, multiple sclerosis, infarction
at the cerebellopontine angle - acoustic neuroma, other tumour
within the petrous bone - spreading middle ear infection
within the cavernous sinus - aneurysm of the internal carotid, tumour or thrombosis of the cavernous sinus

Answer 337

A

compression of the trigeminal nerve results in demyelination and excitation of the nerve resulting in erratic pain signalling

Answer 338

A

almost always unilateral
at least 3 attacks of unilateral facial pain
facial pain occurs in one or more distributions of the
trigeminal nerve, with no radiation beyond the trigeminal distribution
pain

Answer 339

A

pain has at least 3 of the following:
• reoccurring in paroxysmal (sudden and frequent) attacks from a fraction of a second to 2 minutes
• severe intensity
• electric shock like, shooting, stabbing or knife-like
• precipitated by innocuous (non-harmful) stimuli by the affected side of the face e.g. washing or shaving area

Answer 340

A

giant cell arteritis/temporal arteritis should be excluded

- dental pathology, temporomandibular joint dysfunction, migraine, cluster headaches

Answer 341

A

in order to diagnose, there need to be at least 3 attacks with unilateral facial pain
clinical diagnosis based on criteria above and based on history
MRI to exclude secondary causes or other pathologies
not attributed to another disorder

Answer 342

A

typical analgesics and opioids do not work
anticonvulsant suppresses attacks in most patients
other, less effective options e.g. oral phenytoin, gabapentin and lamotrigine
may spontaneously remit after 6-12 months
if drugs fail then surgery may be necessary: microvascular decompression (anomalous vessels are separated from the trigeminal root) or gamma knife surgery (done directly at the trigeminal nerve ganglion or nerve root), stereotactic radiosurgery

Answer 343

A

migraine

4-72 hours
varies

tension type

minutes to days
varies

cluster headache

15-80mins
ECH vs CCH

trigeminal neuralgia

seconds
bouts
many/day

Answer 344

A

migraine

moderate/severe
throbbing
uni/bilateral

tension type

mild/moderate
pressing/tight
uni/bilateral

cluster headache

severe/very severe
boring/hot poker
unilateral

trigeminal neuralgia

severe/very severe
electric/lightening/stabbing
unilateral

Answer 345

A

inflammatory disease of large blood vessels
• systemic immune-mediated vasculitis affecting medium to large size arteries of the aorta and its extra cranial branches
• associated with polymyalgia rheumatica (PMR) and can occur in 50% of cases with GCA

Answer 346

A

primarily in those over 50yrs
most common in caucasians
more common in females than males

Answer 347

A

caucasian
common in elderly women (>60)
polymyalgia rheumatica and giant cell arteritis have a familial component
incidence increases with age

Answer 348

A

there is granulomatous arteritis of unknown aetiology affecting in particular the extra-dural arteries and the large cerebral arteries
arteries become inflamed, thickened and can obstruct blood flow
cerebral arteries affected in particular e.g. temporal artery
opthalmic artery can also be affected potentially resulting in permanent or temporary vision loss

Answer 349

A

severe headaches (temporal pulsating)
tenderness of scalp (combing hair can be painful) or temple
claudication of the jaw (pain in jaw) when eating
tenderness and swelling of one or more temporal or occipital arteries
sudden painless vision loss (emergency); arteritic anterior ischaemic optic neuropathy - optic disc is very pale/swollen
malaise, lethargy, fever
associated symptoms of PMR
dyspnoea, morning stiffness and unequal or weak pulses

Answer 350

A

migraine, tension headache, trigeminal neuralgia, polyarteritis nodosa

Answer 351

A

diagnostic criteria - 3 or more of:
• over 50
• new headache
• temporal artery tenderness or decreased pulsation
• ESR raised
• abnormal artery biopsy - inflammatory infiltrates present

Answer 352

A

diagnostic criteria
normocytic normochromic anaemia
ESR raised
ANCA negative
CRP very high
serum alkaline phosphatase may be raised
temporal artery biopsy

Answer 353

A

definitive diagnostic test
should be taken before or within 7 days of starting high dose corticosteroids
lesions are patchy so take a big chunk

Answer 354

A

cellular infiltrates of CD4+ T lymphocytes, macrophages and giant cells (may not be visible in all cases) in the vessel wall
granulomatous inflammation of the intima and media
breaking up of the internal elastic lamina

Answer 355

A

high dose corticosteroids to stop vision loss; gradual reduction of steroids over 12-18 months
if visual symptoms persist then give IV methylprednisolone for 3 days
used long-term so give GI and bone protection (to prevent osteoporosis due to steroid use) e.g. lansoprazole and alendronate and Ca2+ and
vitamin D
monitor treatment progress by looking at ESR/CRP (should fall)
polymyalgia rheumatica (PMR) presents in 50% of cases with giant cell arteritis

Answer 356

A

C1 (junction with medulla) to L1/L2 (conus medullaris)

Answer 357

A

lumbar and sacral nerve roots are below L1
grouped together to form the cauda equina (final point of the spinal cord)
L1/L2

Answer 358

A

paralysis of both legs; always caused by spinal cord lesion

Answer 359

A

paralysis of one side of the body caused by lesion of the brain

Answer 360

A

contralateral to lesion

Answer 361

A

ipsilateral to the lesion

Answer 362

A

indicate that the lesion is either in the anterior horn cell or distal to the anterior horn cell i.e. in anterior horn cell, plexus or peripheral nerve
decreased muscle tone
wasting (atrophy) +/- fasiculations (spontaneous involuntary twitching)
weakness that corresponds to those muscles supplied by the involved cord segment, nerve root, part of plexus or peripheral nerve
reflexes are reduced or absent

Answer 363

A

can be inferred from the accompanying symptoms
back pain and sciatica suggests a root problem
weakness of the biceps with absence of the biceps reflex, with UMN signs in the legs suggests cord disease e.g. a disc prolapse at C5/C6 - LMN at that level, and UMN below

Answer 364

A

weakness of the biceps with absence of the biceps reflex, with UMN signs in the legs suggests cord disease e.g. a disc prolapse at C5/C6 - LMN at that level, and UMN below

Answer 365

A

slippage of one vertebra over the one below
nerve root comes out above the disc, therefore root affected will be the one below the disc herniation e.g. L4/L5 herniation leads to L5 nerve root compression

Answer 366

A

degenerative disc disease

Answer 367

A

caused by spinal cord compression
UMN signs
spinal cord disease

Answer 368

A

caused by spinal root compression
LMN signs
pain down dermatome supplied by root
weakness in myotome supplied by root
no UMN signs
acute - no LMN signs - since fasciculations and wasting take time to develop

Answer 369

A

C5 - shoulder abduction/biceps jerk
C6 - elbow flexion/supinator jerk
C7 - elbow extension/triceps jerk
L3/4 - knee extension/knee jerk
L5 - ankle dorsiflexion (upwards)
S1 - ankle plantar flexion (downwards)/ankle jerk

Answer 370

A

clavicle - C4
nipples - T4
medial side of arm - T1
umbilicus - T10
anterior and inner leg - L2-3
knee - L4
posterior and outer leg - L5, S1-2
perianal area - S4

Answer 371

A

compression of the spinal cord resulting in upper neurone signs and specific symptoms dependent on where compression is

Answer 372

A

vertebral body neoplasms (most common cause of acute compression) caused by secondary malignancy commonly from lung, breast, prostate, myeloma, lymphoma
spinal pathology (disc herniation and prolapse)

Answer 373

A

when centre of disc (nucleus pulposus) has moved out through the annulus (outer part of disc) resulting in pressure on nerve root and pain

Answer 374

A

when nucleus pulposus moves and presses against the annulus but it doesn’t escape outside the annulus
can produce a bulge in the disc which, sometimes, can result in pressure (less pressure than herniation) on nerve root resulting in pain

Answer 375

A

infection e.g. epidural abscess
haematoma e.g. warfarin
primary spinal cord tumour e.g. glioma, neurofibroma

Answer 376

A

spinal or root pain may precede leg weakness and sensory loss
there is progressive weakness of the legs with UMN signs
onset may be acute (hours to days) or chronic (weeks to months) depending on cause
arm weakness if often less severe e.g. cervical cord lesion
bladder (and anal) sphincter involvement is late and manifests as hesitancy, frequency and later as painless retention
there is sensory loss below the level of the lesion
look for a motor, reflex and sensory level with normal findings above the level of the lesion
LMN signs at the level (especially in cervical cord compression) and UMN below the level - but remember that tone and reflexes are usually reduced initially in acute compression; takes time to develop
depends on the level of the lesion

Answer 377

A

sensory loss below the level of lesion
this is known as the sensory level
sensation abruptly diminishes one/two cord segments below the level of the actual anatomical level of spinal cord compression

Answer 378

A

L5/S1 lesion = S1 nerve root compression

- sensory loss/pain in back of thigh/leg/lateral aspect of little toe (essentially in the sciatic nerve distribution)

Answer 379

A

L4/L5 = L5 nerve root compression:

• sensory loss/pain in lateral thigh/lateral leg and medial side of big toe

Answer 380

A

transverse myelitis, multiple sclerosis, cord vasculitis, trauma, dissecting aneurysm

Answer 381

A

do not delay imaging, since irreversible paraplegia may follow if the cord is not decompressed
speed of imaging should parallel the rate of clinical progression
MRI (gold standard; identifies cause and site of cord compression)
biopsy/surgical exploration may be required to identify the nature of any mass
screening blood tests: FBC, ESR, B12, U+E’s, syphilis serology, LFT, PSA
CXR (looks for TB or malignancy)

Answer 382

A

if malignancy then give IV dexamethasone and consider more specific therapy e.g. radiotherapy or chemotherapy
epidural abscess must be surgically decompressed and antibiotics given
refer to neurosurgeons

Answer 383

A

epidural steroid injection - effective for leg pain
surgical decompression of cord:
laminectomy - removal of the lamina/spongy tissue between discs to relieve pressure and thus symptoms
microdiscectomy - removal of herniated tissue from disc

Answer 384

A

condition that occurs when the bundle of nerves below the end of the spinal cord
medical emergency
cauda equina is formed by the nerve roots caudal (distal) to the level of the termination of the spinal cord at L1/L2
spinal damage at or caudal to L1
flaccid and areflexic weakness

Answer 385

A

a bundle of spinal nerves and spinal nerve rootlets, consisting of the second through fifth lumbar nerve pairs, the first through fifth sacral nerve pairs and the coccygeal nerve, all of which arises from theh lumbar enlargement and the conus medullaris of the spinal cord

Answer 386

A

tapered, lower end of the spinal cord. occurs near lumbar vertebral levels 1 and 2, occasionally lower

Answer 387

A

delicate strand of fibrous tissue, about 20cm in length, proceeding downward from the apex of the conus medullaris
- consists of the filum terminale internum and externum

Answer 388

A

medial reticulospinal tract arises from the pons; it facilitates voluntary movements and increases muscle tone
lateral reticulospinal tract arises from the medulla; inhibits voluntary movements and reduces muscle tone
ipsilateral

Answer 389

A

caudate nucleus and putamen

Answer 390

A

caudate nucleus, putamen, nucleus accumbens, globus pallidus

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Neurology Flashcards

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