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Neurology > Neurosurgery Cortex > Flashcards

Neurosurgery Cortex Flashcards

1
Q

what is the function of the corticobulbar tracts

A

contains UMN of the cranial nerves to provide innervation of the face, head and neck
they innervate the cranial motor nuclei bilaterally
(except the hypoglossal nuclei and the lower facial nuclei which are innervates contralaterally only)

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2
Q

explain the differences between a UMN and LMN facial paly

A

7th CN nucleus in pons
upper half of nucleus= upper half of face and same for lower and lower
upper half of nucleus receive motor input bilaterally, lower half of nucleus recieves only contralateral info

UMN will have paralysis of contralateral lower facial muscles with forehead sparing (as info from other side)= central facial palsy

LMN will have paralysis of the ipsilateral half of the face= bells palsy

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3
Q

what tracts originate from the brainstem and control involuntary movements

A

extra-pyramidal

  • vestibulospinal
  • reticulospinal
  • rubrospinal
  • tectospinal
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4
Q

what is the role of the vestibulospinal tract, and where does it originate

A

originates from the vestibular nucleus in the pons

it controls balance and posture by innervating the antigravity muscles (extensor for legs, flexor for arms)

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5
Q

what is the origin and function of the reticulospinal tract

A

Originates from the reticular formation in the medulla and pons:
The pontine reticulospinal tract facilitate voluntary/reflex responses and increases tone.
The medullary reticulospinal tract inhibits voluntary/reflex responses and decreases tone (think dulling down)

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6
Q

what is the origin and function of the rubrospinal tract

A

Originates from the red nucleus in the midbrain. It excites flexor muscles and inhibits extensor muscles of the upper body.

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7
Q

what is the origin and function of the tectospinal tract

A

Originates from the superior colliculus in the midbrain. It co-ordinates movements of head and neck to vision stimuli.

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8
Q

how many vertebrae all together

A

33

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9
Q

what does C1 lack

A

a spinous process or body

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10
Q

what is different about C2

A

has dens (ondontoid process)

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11
Q

what is different about C3-4

A

have short and bifid spinous processes

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12
Q

where does the posterior ligament run

A

within vertebral canal, posterior to the vertebral bodies

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13
Q

what does the ligamentum flavum do

A

It runs vertically connecting the lamina of adjacent vertebrae. It helps maintain an upright posture and assist straightening the spine after flexion.

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14
Q

where are LP done

A

L3/4

L4/5

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15
Q

what are the layers a needle has to go through in an LP

A 
skin 
fascia 
supraspinous lig
interspinous lig
ligamentum flavum 
epidural space 
dura
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16
Q

what is the usual age range for mechanical back pain

A

20-55

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17
Q

when is mechanical back pain worse

A

morning stiffness which resolves with movement

pain is made worse by prolonged sitting or when rising from a seated position

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18
Q

what can happen when facet joints are hypertrophied

A

patients will get referred pain from the nerve supplying the facet join that mimics sciatica, but doesn’t radiate below the knee

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19
Q

describe a paramedian prolapse

A

aka posterolateral
most common
compresses travering disc

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20
Q

describe a far lateral prolapse

A

aka extraforaminal

compress the exiting nerve

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21
Q

what can a central/ medial herniation cause

A

lumbar stenosis or if large enough CES

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22
Q

what is radiculopathy

A

dysfunction of a nerve root causing dermatomal sensory deficit with weakness of the muscle groups supplied by the nerve

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23
Q

what is sciatic pain like

A

Shooting pain radiating from the buttocks down to the posterior knee/leg. The pain can be exaggerated by coughing or sneezing.

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24
Q

what does a straight leg raise test positive mean

A

with the patient lying down on their back, lift the patient’s leg while the knee is straight. If the angle to which the leg can be raised before eliciting the patient’s sciatic pain is <45° then the test is said to be positive.

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25
Q

what are the clinical features of an L5/S1 prolapse disc involing S1 root

A

Pain along the posterior thigh with radiation to the heel.
Weakness of plantar flexion (on occasion).
Sensory loss in the lateral foot.
Reduced or absent ankle jerk.

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26
Q

what are the clinical features of an L4/5 prolapse affecting L5

A

Pain along the posterior or posterolateral thigh with radiation to the dorsum of the foot and great toe.
Weakness of dorsiflexion of the toe or foot.
Paraesthesia and numbness of the dorsum of the foot and great toe.
Reflex changes unlikely.

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27
Q

what are the clinical features of an L3/4 prolapse affecting L4

A

Pain in the anterior thigh.
Wasting of the quadriceps muscle.
Weakness of the quadriceps function and dorsiflexion of foot.
Diminished sensation over anterior thigh, knee and medial aspect of lower leg.
Reduced knee jerk.

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28
Q

what are the indications for a discectomy following a prolapse

A

Failure of conservative treatment (physiotherapy and analgesia) - First line management
Pain
Central disc prolapse: Patients with bilateral sciatica or other features indicating a central disc prolapse, such as sphincter disturbance and diminished perineal sensation, should be investigated promptly.
Tumour
Neurological deficits

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29
Q

if what reflex is present does it make it unlikely to be CES

A

ankle

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30
Q

Tx for CES

A

emergency MRI lumbosacral
PR
If it was due to a herniated disc –> discectomy
If it was due to a fracture –> decompression +- fixation
If it was due to a hematoma –> evacuation

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31
Q

what are the clinical features of spinal stenosis

A

Unilateral or bilateral hip, buttocks or lower extremity pain or burning sensation precipitated by standing or back extension and relieved by sitting, lumbar flexion or walking uphill (patients can often develop an “anthropoid posture” which is exaggerated flexion of the waist).
Neurogenic intermittent claudication: leg weakness, tingling and numbness which can be accompanied by paresthesia.
insidious progressive disease

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32
Q

what is sclerotomal

A

muscle group with the same vascular supply (distribution of symptoms in vascular claudication)

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33
Q

what is the difference in pain in neural and vascular claudication

A

neural- burning

vascular- cramping

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34
Q

what investigation to diagnose neurogenic claudication

A

MRI lumbosacral spine

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35
Q

what is the treatment for neurogenic claudication

A

If symptoms are tolerable and the walking distance is not significantly affected then conservative treatment is offered first (physiotherapy and analgesia). Symptoms usually worsen slowly in a predictable manner and surgery should be offered electively when the patient’s symptoms become intolerable and oral analgesia is no longer sufficient. Lumbar surgical decompression (lumbar laminectomy) is the preferred surgical treatment.

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36
Q

what is cervical spondylosis and how can it present

A

a degenerative arthritic process involving the cervical spine

mainly >50s
either present as degenerative cervical myelopathy (UMN signs) or radiculopathy (LMN signs).

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37
Q

what is seen radiologically in cervical spondylosis

A

Narrowing of the disc space (the C5/C6 and C6/C7 levels are the most commonly affected)
Osteophyte formation

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38
Q

what is the Tx for cervical spondylosis

A

surgery:

  • decompressive cervical laminectomy
  • discectomy
  • cervical foraminotomy
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39
Q

what causes myeopathy and what is the result

A

can result from a spinal cord compression which causes UMN signs with symptoms more prominent in the lower limbs

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40
Q

what are the clinical features of degenerative cervical myelopathy

A

older patients
progressive
imbalance and disturbance of gait/ falls (due to hypertonia and decreased proprioception)
clumsy hands
incontinence (rare)
non dermatomal pain
jumping legs at night due to hyperreflexia

weakness, spasticity
+ve babinski and hoffmans

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41
Q

what imaging for degenerative cervical myelopathy

A

MRI gold standard

  • disc degeneration
  • ligament hypertrophy
  • spinal cord signal chance
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42
Q

Tx for degenerative cervical myelopathy

A

decompressive spinal surgery (prevent deterioration)

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43
Q

what is anterior cord syndrome

A

Cord infarction by the area supplied by the anterior spinal artery.
It produces paralysis and loss of pain and temperature below the level of injury with preserved proprioception and vibration sensation.

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44
Q

where does the contralateral loss of pain and temp begin in brown sequard

A

1 or 2 segments below the lesion

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45
Q

what causes central cord syndrome

A

Acute extension injury to already stenotic neck or syringomyelia or tumour

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46
Q

what are the symptoms of central cord syndrome

A

Predominantly bilateral upper limb weakness>lower limb (the fibers supplying the upper limbs in the lateral corticospinal tracts are more medial to the fibers supplying the lower limbs, hence a lesion in the central cord is more likely to damage the upper limb fibers).
“Cape-like” spinothalamic sensory loss (pain and temperature).
Dorsal Columns preserved.

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47
Q

how do you remember what rubrospinal tract does

A

think of a bro flexing his biceps

-excites flexors, inhibits extensors of the upper limb

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48
Q

explain decorticate vs decerebrate postures

A

Corticospinal most dominant motor tract, then ruborospinal
When don’t have corticospinal tract innervation, rubro will take over (flexion of upper limbs)= decorticate
When rubro knocked out reticulo happens (extension of upper and lower limbs)= decerebrate

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49
Q

what posture will result from a lesion above the level of the midbrain

A

decorticate- rubrospinal in tact as red nucleus in midbrain, cortico not working

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50
Q

what posture will result from a lesion below the midbrain

A

decerebrate = cortico and rubro tracts not working so reticulo (originates in pons/ medulla) takes over

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51
Q

how does the DCML reach the post central gyrus

A

decussate in medulla to the contralateral medial leminiscus to reach the primary somatosensory area

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52
Q

describe the 3 order neurones in the DCML

A

1st order neurone travel from site of excitation to dorsal sensory ganglion in spinal cord root. 2nd enters dorsal column and ascend entirety of cord crossing to the other side then thalamus where it synapses. 3rd – thalamus to post central gyrus

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53
Q

A 30 year old man presented with a stab wound in his back. He has right sided weakness starting at T5 and left sided loss of pinprick sensation and temperature starting at T7.

what cord compression syndrome

A

brown sequard

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54
Q

A 39-year-old woman presented with severe headaches whenever she sneezed. She also had decreased sensation to pinprick over her upper back, shoulders, and upper arms. Her power in her arms was 2/5 but her lower body power was 5/5.

what spinal cord compression syndrome

A

syringomyelia (type of central cord syndrome)

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55
Q

what is syringomyelia

A

when a cysts forms on the spinal cord and compresses it

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56
Q

what are the dural venous sinuses

A

between the two layers of dura mater

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57
Q

what is the outer layer of dura mater adherent to

A

periosteum

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58
Q

what is the cerebellum derived from embryologically

A

telencephalon

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59
Q

what does the middle frontal gyrus in the frontal lobe do

A

contains the frontal eye fields which control contralateral voluntary eye movements

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60
Q

what does the inferior frontal gyrus in the frontal lobe do

A

contains bocas speech area (in the dominant hemisphere)

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61
Q

what does damage to brocas area produce

A

expressive dysphagia

can comprehend words but produce faulty sentences and phonemic errors

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62
Q

what does damage to the inferior parietal lobule cause

A

nominal aphasia (problems recalling words, names and numbers

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63
Q

what does the superior temporal gyrus contain

A

the auditory area of the cortex

wernickes speech area (in dominant hemisphere)

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64
Q

what does damage to wernickes area cause

A

receptive dysphasia - impaired comprehension, produces jargon ‘word salad) but speech fluent

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65
Q

where is the visual cortex

A

occipital lobe

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66
Q

where is the insula

A

lies deep within the lateral sulcus

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67
Q

what is the role of the limbic system

A

higher emotional functions

contains major component of the memory system

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68
Q

where is the limbic system

A

medial hemisphere surface, encircles the corpus callosum

important structure include the cingulate gyrus and the hippocampus

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69
Q

what is the cerebellum derived from embryologically

A

the metencephalon

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70
Q

what separates the cerebrum from the cerebellum

A

tentorium cerebelli

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71
Q

what is the vermis

A

midline structure which connects the two hemispheres of the cerebellum

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72
Q

what are the three components of the cerebellum and their functions

A

vestibulocerebellum - receives input from the vestibular organs for the maintenance of balance and coordinating vestibule-ocular reflexes

spinocerebellum- maintains muscle tone and participates in posture and gait

cerebrocerebellum- coordination of voluntary motor activity, corrects any error in the movements to ensure they are smoothly executed

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73
Q

what is scanning dysarthia

A

when a patient speaks slowly with poor articulation of speech - caused by cerebellar dysfunction

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74
Q

what parts of brain are derived from the diencephalon

A

thalamus
hypothalamus
subthalamus
epithalamus

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75
Q

what does the thalamus do

A

involved in maintaining consciousness
modulates motor function- has reciprocal connections with the motor cortex, basal ganglia and cerebellum
is a relay station for all all sensory impulses (e.g. lateral geniculate nucleus is a relay between retina and visual cortex)

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76
Q

what can a thalamic infarction cause

A

hemiparesis, spontaneous pain, hemichorea, severe impairment of consciousness

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77
Q

what does the hypothalamus do

A

influences autonomics, endocrine and limbic system

  • thermal regulation
  • regulates release of hormones from adenohypophysis
  • synthesis ADH and oxytocin (projects to the neurohypophysis)
  • regulates feeding and starvation
  • contains mamillary nucleus which receives information from the hippocampal formation
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78
Q

what nucleus is affected in wernickes encephalopathy

A

mamillary nucleus

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79
Q

what deficiency causes wernickes

A

B1 (thiamine)

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80
Q

what characterises korsakoffs

A

anterograde amnesia and confabulation

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81
Q

how do patients with wernickes present

A

confusion, ataxia and nystagmus

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82
Q

what do subthalamic lesions cause

A

contralateral hemiballism (chorea)

subthalamus is closely connected to the basal ganglia

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83
Q

what does the basal ganglia contain

A

caudate nucleus, putamen and globus pallidus

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84
Q

what is the role of the basal ganglia

A

exert both excitatory and inhibitory effects of the motor cortex
initiate and facilitate movement
control muscle tone

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85
Q

what do lesions in the basal ganglia cause

A

alteration in muscle activity or tone

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86
Q

what are alpha-synuclein containing inclusions

A

lewey bodies

present in parkinsons

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87
Q

what gene causes huntigtons

A

CAG trinucleotide repeats - increase from generation to generation (genetic anticipation)

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88
Q

what five different symptoms do tumours of the CNS present with

A

progressive focal neurological deficits

HA- worse on lying down, associated with N&V due to increase ICP

seizures

gradual cognitive slowing and personality changes

endocrine disturbances in pituitary or hypothalamic tumours

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89
Q

what symptoms might a lesion in the frontal lobe cause

A

contralateral weakness (motor cortex)
personality changes
urinary incontinence (micturition inhibition centre)
gaze abnormalities (frontal eye fields)
expressive dysphagia/ aphasia (brocas area)
seizures

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90
Q

what symptoms might a lesion in the temporal lobe cause

A

memory deficits
receptive aphasia/ dysphagia (wernickes area)
contralateral supeiror quadrantopia
seizures

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91
Q

what symptoms might a lesion in the parietal lobe cause

A

contralateral weakness and sensory loss (primary somatosensory cortex)
contralateral inferior quadrantopia

if domininant lobe affected: dyscalculia, dysgraphia, finger agnosia, left and right disorientation

if non dominant lobe affected: neglect (deficit in awareness of one side of body), dressing apraxia and constructional apraxia

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92
Q

what symptoms might a lesion in the occipital lobe cause

A

contralateral homonymous hemianopia

visual hallucinations

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93
Q

what symptoms might a lesion in the cerebellum cause

A 
ipsilateral ataxia 
N&amp;V
dizziness and vertigo 
slurred speech 
intention tremor
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94
Q

what is the WHO grading for gliomas

A

I- no morphological features
II- atypia alone
III- atypia and mitosis
IV- atypia and mitosis with vascular proliferation/ necrosis

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95
Q

what is the most common primary brain tumour

A

high grade gliomas

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96
Q

what are high grade gliomas

A

either WHO grade II (anaplastic astrocytomas) or grade IV glioblastoma multiforme (GBM)

of these GBM more frequent

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97
Q

who gets glioblastoma multiforme tumours

A

older people

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98
Q

where do GBM tumours arise

A

in cerebral hemispheres - most commonly in temporal, parietal and frontal lobes

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99
Q

what imaging for glioblastomas

A

MRI

seen as heterogeneously enhancing SOL, with areas of necrosis, can have a butterfly appearance

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100
Q

what is done if an MRI shows a high grade glioma

A

biopsy taken for prognosis and MGMT promoter and methylation test (predictive repsonse alkylating agent chemo (temozolamide)

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101
Q

what is the treatment for gliobastomas

A

Stupp protocol:
-surgery + radiotherapy +/- chemo (e.g. temozolamide)
can improve median survival to 14 months

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102
Q

what are low grade gliomas

A 
slow growing primary brain tumours 
grades I (pilocytic astrocytomas) and II (diffuse astrocytoma/ oligodendrogliomas)
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103
Q

who gets low grade gliomas

A

children and adults

most common in 2nd and 3rd decades

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104
Q

who gets pilocytic astrocytomas (a type of low grade glioma)

A

children and young adults

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105
Q

what is the prognosis for a pilocytic astrocyoma

A

high cure rate after maximal resective surgery +/- adjuvant therapy

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106
Q

what is the most common low grade glioma

A

pilocytic astrocytoma

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107
Q

what is the histology of a pilocytic astrocytoma

A

bipolar cells with long hair like projections

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108
Q

where do pilocytic astrocytomas occur

A

cerebellum and midline structures (thalamus, optic chiasm)

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109
Q

what condition are optic pathway gliomas common in

A

neurofibromatosis type 1

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110
Q

where do you get diffuse astrocytomas

A

cerebral hemispheres, esp frontal and temporal lobes

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111
Q

who gets a diffuse astrocytoma and how do they present

A

young adults
are slow growing - can progress to higher grades
commonly present with seizures

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112
Q

what is the treatment for diffuse astrocytomas

A

maximal resective surgery + chemo/ radiotherapy

can double life expectancy to beyond 15 years

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113
Q

which low grade glioma has the best prognosis

A

oligodendrogliomas

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114
Q

where do you get oligodendrogliomas

A

affect the frontal lobe of the cerebral hemisphere, white matter, cortex
can invade subarachnoid space

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115
Q

who gets oligodendrogliomas and how do they present

A

25-45 y/o’s

seizures and headaches

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116
Q

what are meningiomas

A

common benign extra-axial
(external to brain parenchyma) intracranial tumours that grow slowly, are well demarcated and do not usually infiltrate the brain

(originate from arachonid cap cells in arachoid membrane)

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117
Q

who gets meningiomas

A

elderly patients - 6th/7th decade
females slightly more
NF type 2
childhood radiation exposure

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118
Q

how do meningiomas present

A

usually asymptomatic and are found incidentally on imaging
if symptoms develop, then it will correlate with the site of the brain that is affected. The most common presenting complaint however is headache then symptoms of increased intra-cranial pressure can follow.

A meningioma in the olfactory groove can lead to Foster Kennedy syndrome which is clinically defined as optic atrophy in the ipsilateral eye and papilloedema in the contralateral eye

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119
Q

what is the difference between micro and macroadenomas (pituitary tumours)

A

macro larger than 10mm in diameter

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120
Q

are the majority of pituitary tumours malignant or benign

A

benign - arise from cell types in anterior lobe of pituitary gland

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121
Q

how do most pituitary tumours present

A

endocrine dysfunction

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122
Q

what is the treatment for prolactinomas

A

dopamine agonists- cabergoline

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123
Q

what is a high dose dexmethasone suppression test used to determine

A

adrenal or pituirary causes of cortisol excess

high dose will suppress pituitary causes only

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124
Q

what are thyroid hormones like in a thyrotropinoma (pituitary tumour)

A

TSH high, free T3 and free T4 high

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125
Q

what is used to shrink GH secreting pituitary tumours before surgery

A

pegvisomant and somatostatin analogues- octreotide

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126
Q

when is radiotherapy used for pituitary tumours

A

when too large to operate/ growing into cavernous sinus

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127
Q

what tests should you do if you suspect a pituitary tumour

A

early morning cortisol and prolactin

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128
Q

what are acoustic neuromas/ vestibular schwannomas

A

benign tumours derived from schwann cells

arise in cerebellopontine angle and affect the vestibular portion of cranial nerve 8

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129
Q

what should you suspect with bilateral accoustic neuromas in the young

A

NF 2

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130
Q

what is the pathology of vestibular schwannomas

A

Verocay bodies can be seen, which are palisading nuclei against a fibrillary background

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131
Q

what is the presentation of an acoustic neuroma

A

30-50 y/os
unilateral SNHL, tinnitus and vertigo
if big can have headache
facial pain/ numbness- if CN V involved

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132
Q

what is the management for vestibular schwannomas

A

serial observation- hearing aid, MRI, neuro exams

sterotatic radiosurgery

microsurgical excision

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133
Q

what are haemangioblastoma

A

benign, cystic, highly vascular tumours

develop in posterior fossa

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134
Q

what is the presentation of a haemangioblastoma

A 
cerebral dysfunction (occur in post fossa)
symptoms of raised ICP

associated with von hipple-landau syndrome - multiple haemangiomas which may be symptomatic (retinal angiomas, renal cell carcinoma and phaeochrmomcytoma)

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135
Q

what should GH levels be after oral glucose (100g)

A

less than 1mg/ml

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136
Q

what definitive test for acromegaly

A

IGF-1

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137
Q

what does the anterior intracranial circulation arise from

A

the internal carotids

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138
Q

what does the posterior intracranial circulation arise from

A

paired vertebral arteries- join to form basilar

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139
Q

what makes up the anterior circulation of the brain

A

internal carotid
ACA
MCA
anterior communcicating artery

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140
Q

where does the internal carotid arise from

A

common carotids at carotid bifurcation (C4)

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141
Q

what is the path of the internal carotid

A

enters the base of the skull through the carotid canal

transverses the foramen lacerum (does not pass through it)

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142
Q

what are the branches of the internal carotid

A

ophthalmic
anterior choroidal
posterior communicating

terminates into bifurcation into MCA and ACA

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143
Q

what is the path of the ACA

A

arches over corpus callosum in the longitudinal fissure

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144
Q

what does the ACA supply

A

medial part of left and right cerebral hemispheres, back to the parietal lobes
most of corpus callosum
anterior limb of internal capsule
part of caudate nucleus

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145
Q

is the MCA or ACA bigger

A

MCA

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146
Q

what is the path of the MCA

A

extends from the internal carotid to the sylvian fissure

exits fissure onto lateral surface of hemisphere

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147
Q

what does the MCA supply

A

majority of the lateral hemisphere, basal ganglia and internal capsule

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148
Q

what does the posterior circulation of the brain consist of

A

vertebral artery
basilar
PCA
posterior communicating

149
Q

what does the vertebral artery arise from

A

subclavian artery

150
Q

what is the path of the vertebral artery

A

extends through the transverse foramen of the cervical vertebrae (C6 to C2)
join to form basilar

151
Q

what is the main branch of the vertebral arteries

A

posterior inferior cerebellar arteries

152
Q

what do the posterior inferior cerebellar arteries supply

A

posteroinferior cerebellar hemispheres

153
Q

what is the path of the basilar artery

A

vertebral arteries combine at the base of the pons
courses superiorly towards the midbrain
terminates at interpeduncular cistern - goes into two posterior arteries

154
Q

what are the branches of the basilar artery

A

anterior inferior cerebellar artery
pontine branches
superior cerebellar artery

155
Q

what does the anterior inferior cerebellar artery supply

A

the anterolateral part of the cerebellum

also gives off the labyrinthine artery which supplies the inner ear

156
Q

what does the superior cerebellar artery supply

A

superior aspect of the cerebellum

157
Q

what is the path f the posterior cerebellar artery

A

goes backwards towards the occipital lobe

158
Q

what does the posterior cerebral artery supply

A

occipital cortex

gives of branches to supply the thalamus

159
Q

what does the posterior communicating artery branch from

A

the internal carotid

160
Q

what are the two components of the brains venous system

A 
cerebral veins (superficial and deep) 
dural venous sinuses
161
Q

why do the dural venous sinuses have arachnoid granulations

A

to allow CSF to be reabsorbed from subarachnoid space into venous system

162
Q

what is the path of the superior sagittal sinus

A

(dural sinuses within two layers of dura mater) runs from the anterior aspect of the falx cerebri
terminates at the confluence of sinuses (is joined by straight sinus)
from here blood drains into left and right venous sinuses and then into internal jugular vein

163
Q

where do cerebral veins drain to

A

dural sinuses
superficial veins -> superior sagittal sinus
deep veins -> straight sinus

164
Q

what is a common cause of haemorrhage in young adults

A

arteriovenous malformation

165
Q

what causes AVM

A

congenital

166
Q

what are the clinical features of AVMs

A

usually asymptomatic
can cause:
-(most common) haemorrhage (most commonly intracerebral, but can be intraventricular or subarachnoid aswell)
-2nd= seizures can be generalised or complex partial
-progressive neurological deficit (e.g. slowly progressive hemiparesis (due to local ischaemia- steal phenomenon)
-headaches - unilateral and throbbing/ more generalised

167
Q

what Ix for AVMs

A

catheter angiography
-shows feeding arteries supplying the nidus and veins draining it

CTA can be used in emergencies

168
Q

what is seen on Ix of AVMs

A

tangle of vessels
large feeding artery
large draining veins

169
Q

what is the management of AVMs

A

surgery
-open craniotomy and excision

if risks of surgery high and AVM small/ deep then stereotactic radiosurgery (takes 1-3 years to work)

if AVM in deep tissue/ eloquent area and inaccessible to surgery then endovascular coiling

observation if very large AVM/ in eloquent areas of the brain

170
Q

what is the most common cause of sub arachnoid haemorrhage

A 
head trauma
berry aneurysm (most common non traumatic cause)
171
Q

what increases the risk of a SAH

A

large aneurysm
location- higher in posterior circulation
FHx of PKD
HPTx
co-morbidity- smoking, connective tissue disease

172
Q

what are the clinical features of SAH

A

sudden onset thunderclap headache - can last hours- days
neck stiffness and photophobia- meningeal irritation
N&V- raised ICP/ meningeal irritation

a third nerve palsy can occur due to posterior communicating artery aneurysm
confusion, seizures, LOC
vitreous haemorrhage

173
Q

what runs in the subarachnoid space

A

CSF and vessels

174
Q

where do subarachonoid haemorrhages happen

A

between arachonoid and pia

175
Q

is an SAH arterial or venous

A

arterial

176
Q

what investigations for SAH- what is seen

A

CT
(if CT normal for example if it was delayed after SAH a LP should be done)
CT angiogram gives you a definitive diagnosis, shows location and route for endovascular coiling

CT- hyperdense signal in subarachnoid space
LP- xanthochromia (yellow discolouration of CSF)

177
Q

what is the management for SAH

A

endovasuclar coiling

craniotomy and microsurgical clipping of aneurysm can be considered if large MCA aneurysm rupturs/ associated clots

178
Q

what are the common complications of SAH

A

vasospasm- prolonged arterial contraction, leading to delayed ischaemic neurologicla deficit, 3-14 days post haemorrhage. treated with nimodipine)
re-bleed- 2 weeks post, more common in elderly/ HPTX, managed with surgical clipping/ coiling
hydrocephalus
seizures
hyponatraemia

179
Q

what is cavernous malformation

A

benign vascular lesion in the sinusoidal spaces
are lined by endothelium, separated by elastin
look in a mulberry
no intervening brain parenchyma
are low flow lesions (unlike AVM)
hard to visualise on angiography
can be familial (usually multiple) or sporadic

180
Q

what are the clinical features of cavernous malformation

A

seizures
progressive neurological deficit
haemorrhage (can be recurrent and cause neuro symptoms. seizures)

181
Q

what Ix for caverous malformations

A

CT- good for acute haemorrhage
MRI T2- gold standard (focal popcorn lesion, surrounded by ring of hypo-intensity = hemosiderin deposition)
angiography- not helpful but can rule others out

182
Q

what management for a cavernous malformation

A

observe

surgical excision

183
Q

where is a subdural haemorrhage

A

between the dura and arachnoid

184
Q

is a chronic subdural haemorrhage arterial or venous

A

venous (cerebral bridging veins)

185
Q

what is the presentation of a chronic subdural haemorrhage

A

older patients, recurrent low impact trauma

progressive headache and confusion

186
Q

what is seen on CT in chronic subdural haemorrhage

A

hypodense crescent shaped appearance (blood is old)

187
Q

where is an extradural haemorrhage

A

between skull and dura

188
Q

what vessels usually causes an extradural haemorrhage

A

aterial- middle meningeal artery (under pterion)

189
Q

what is the presentation of an extradural haemorrhage

A

young patients head trauma

lucid intervals followed by unconsciouness

190
Q

what is seen on CT in a extradural haemorrhage

A

hyperdense biconvex lens appearance

191
Q

what can a subdural hematoma not cross

A

falx or tentorium

192
Q

what are the possible symptoms of cerebral hernitation

A

Extensor response
Cushing’s triad: hypertension, bradycardia and irregular breathing (damage to the medulla from herniation)
Unreactive pupil (uncal herniation) (oculomotor nerve runs close to the uncus- get palsy)

193
Q

A patient presents unconscious with unilateral pupil mydriasis that does not constrict to light following a car accident. On CT, an intracranial hemorrhage with cerebral herniation. What is the most likely type of herniation

A

uncal herniation

194
Q

what diseases are associated with aneurysms

A

PKD
fibromusclar disease
ehlers danlos

195
Q

what increases risk of aneurysm rupture

A 
old age
female
smoking
previous aneursymal SAH
large aneurysms 
hypertension
196
Q

what is the most common type of cerebral aneurysm causing a SAH

A

berry aneurysm (aka saccular)

197
Q

what are fusiform and mycotic aneurysms

A

fusiform- occur in intracranial (esp basilar and ICA), due to atheromatous degeneration, associated with hypertension

mycotic due to septic emboli

198
Q

what nerves can an unruptured posterior communication artery aneurysm compress

A

oculomotor nerve- 3rd nerve palsy (ptsosis, extraocular palsy)

199
Q

what nerves can an unruptured anterior communication artery aneurysm compress

A

if large compresses optic chiasm

200
Q

what symptom can an unruptured basilar artery aneurysm cause

A 
headache
3rd nerve palsy 
confusion 
hemiparesis 
menignism 
drowsiness 
diplopia 
nausea 
vomiting
201
Q

what is the treatment of aneurysms

A

if symptomatic can do endovascular coiling/ neurosurgical craniotomy + clipping of the aneurysm

202
Q

where can a TIA happen

A

in brain, spinal cord and retina

203
Q

what are the risk factors for a TIA

A 
Prior TIA or stroke
Hypertension
Atrial fibrillation
Diabetes 
History of ischaemic heart disease
Smoking
204
Q

what are the clinical features of a TIA

A

Cortical symptoms: facial or limb weakness, sensory disturbance, …
Speech abnormalities: dysphasia or dysarthria
Visual disturbance: visual field defects or amarousis fugax
Cranial nerve involvement
Memory disturbance

205
Q

what score can be used to identify whether patients with a TIA are at low or high risk of developing subsequent cerebrovascular injuries

A

ABCD2
Scores of 0-3 points to a low risk subsequent stroke and scores >4 are higher risk subsequent strokes.
includes age, BP. clinical features (any other symptoms= 0, speech= 1, limb weakness= 3)
duration
diabetes
Patients with a score >4 should be referred to a stroke specialist within 24 hours. Patients with a lower risk should be assessed and treated within 7 days of symptoms onset.

206
Q

what Ix for TIAs

A 
FBC: to identify any blood disorders
Renal function: chronic renal failure
Glucose: diabetes
ESR: giant cell arteritis or other vasculitis
ECG: atrial fibrillation 
Specific investigations:

MRI: to look for ischaemic brain damage
Carotid doppler: if carotid stenosis is suspected

207
Q

what scan to identify a haemorrhagic stroke

A

CT

208
Q

what happens biologically when blood supply to brain is cut off

A

glucose and oxygen transport to neurones decreases. Glutamate and proteolytic enzymes release causes the formation of cerebral oedema and inflammation which would lead to worsening ischaemia to adjacent neurones and widening of the circle of cell death

209
Q

what is a penumbra

A

area of non-functioning yet reversible damage to tissue that if left untreated would lead to an irreversible change to the cells.

210
Q

what are the types of dyspahgia

A

wernickes - receptive
brocas- expressive
conductive- damage to the arcuate fasciculus that connects Broca to Wernicke

211
Q

what are the common visual symptoms of a stroke

A

contralateral homonymous hemianopia
visual inattention- failure to detect visual stimulus in one half of the visual field when both are testes together, can detect when half tested on their own

212
Q

decribe the innervation to facial muscles

A

CN7
facial nerve nuclei receive bilateral cortical innervation to upper part of face, contralateral innervation to lower face

213
Q

what are lacunar infarcts

A

pure motor or sensory stroke/ an ataxic hemiparesis

214
Q

what does a total anterior circulation infarct have

A
  1. higher cerebral dysfunction (e.g. dysphagia)
  2. homonymous visual defect
  3. ipsilateral motor and/ or sensory deficit of at least two areas out of face, arm and leg
215
Q

what does a partial anterior circulation infarct have

A

two of TACI features:

  1. higher cerebral dysfunction (e.g. dysphagia)
  2. homonymous visual defect
  3. ipsilateral motor and/ or sensory deficit of at least two areas out of face, arm and leg
216
Q

what does a posterior circumlocution infarct have

A

any of:

  • Ipsilateral cranial nerve palsy with contralateral motor and/or sensory deficit
  • Bilateral motor and/or sensory deficit
  • Cerebellar dysfunction
  • Isolated homonymous visual field defect
217
Q

Tx for ischaemic stroke presenting within 4.5 hrs

A

intravenous thrombolysis (alteplase). Stroke affecting the carotid territory should be evaluated for carotid endarterectomy.

Some patients with an MCA infarct + cerebral oedema can be considered to be treated with a hemicraniectomy within 48 hours.

Aspirin 300 mg daily should be commenced within hours of ischaemic stroke and continued for two weeks then patients should be transferred to clopidegrol for life (patients who are not suitable for clopidegrol can be put on low dose aspirin (75 mg)+dipyridamole). In Atrial Fibrillation patients, warfarin can be re-introduced after 2 weeks following a major stroke.

218
Q

what lobes might be affected in an anterior circulation stroke

A

frontal, parietal and temporal

219
Q

what is the role of the brain stem

A

swallowing, breathing, heartbeat, consciouness

220
Q

what is a role of the parietal lobe

A

comprehension of language

221
Q

where is the primary auditory cortex

A

superior temporal gyrus

222
Q

where is brocas area

A

inferior frontal gyrus

223
Q

where is wernickes area

A

superior temporal gyrus/ temporo-parietal area

224
Q

where in brain does thermoregulation

A

hypothalamus

225
Q

where is the primary visual cortex

A

occipital lobe

226
Q

where is the primary motor cortex

A

precentral gyrus

227
Q

where is the primary somatosensory cortex

A

postcentral gyrus

228
Q

where is the oculumotor nucleus

A

midbrain

229
Q

A 40 year old right-handed accountant presents with difficulty in writing and that he ”wasn’t as good with numbers as before”. On examination, he had a left-right disorientation. Imaging and biopsy confirmed the presence of a meningioma.
where is the lesion

A

left parietal lobe- gestern syndrome (dominant parietal lobe lesion)

230
Q

what is a common presentation in cavernous malformations

A

new onset seizure

231
Q

what part of brain does the optic nerve transmit to

A

occipital lobe

232
Q

what branches of optic nerve decussate at chiasm

A

nasal

233
Q

what comes after the optic chiasm

A

the optic tracts

234
Q

what connects the optic tracts to the chiasm

A

lateral geniculate nucleus

235
Q

what does the optic tract convey

A

info from contralateral nasal and ipsilateral temporal retina
left tract will be right side of vision

236
Q

where do fibres that serve the afferent limb of the pupillomotor reflex exit the optic pathway

A

leave optic tracts to terminate in the pretectal nuclei in midbrain
then projects to edinger westphal nuclei

237
Q

what do the optic radiations do

A

connect the lateral geniculate nuclei to the visual cortex in the occipital lobe

238
Q

where do the different parts of the optic radiations end up

A

Superior optic radiations pass through the parietal lobe and end superiorly to the calcarine sulcus

inferior optic radiations (Meyer’s loop) pass through the temporal lobe and end inferiorly to the calcarine sulcus

239
Q

where is the macula represented in the brain

A

lateral to the tip of the calcarine sulcus

240
Q

where is the oculomotor nucleus

A

located in the dorsal midbrain at the level of the superior colliuculus

241
Q

what supplies the levator muscle of the eyelid

A

oculomotor

242
Q

what is the path of the oculomotor nerve

A

through the interpeduncular fossa
passes between the posterior cerebral artery and superior cerebellar artery
travels through lateral wall of cavernous sinus
enters orbit through superior orbital fissure

243
Q

what fibres from the EW nucleus accompany the oculomotor nerve- what do they do

A

parasympathetic fibres

innervate the sphincter papillae and ciliary muscles

244
Q

where is the troclear nuclei

A

in midbrain at the level of the inferior colliculus

245
Q

how does the trochlear nerve enter to orbit

A

passes through lateral wall of the cavernous sinus inferior to the oculomotor nerve and enters the orbit through the superior orbital fissure

246
Q

what is unique about the trochlear nerve

A

It is the only cranial nerve that exits dorsally from the brainstem.
It is the smallest cranial nerve.
Has the longest intracranial course.

247
Q

what is the course of the abducens nerve

A

travels through the cavernous sinus lateral to the internal carotid. It then enters the orbit via the superior orbital fissure to innervate the lateral rectus (abduction).

248
Q

what cranial nerve originates from the telenecephalon

A

olfactory

249
Q

what cranial nerve originates from the diencephalon

A

optic

250
Q

what cranial nerves originate from the midbrain

A

oculomotor and trochlear

251
Q

what cranial nerves originate from the pons

A

trigeminal

abducens

252
Q

what cranial nerves originate from the pons at the cerebellopontine angle

A

facial

vaestibulocochlear

253
Q

what cranial nerves originate from the medulla

A

glossopharyngeal
vagus
accessory
hypoglossal

254
Q

what are the cranial origins for each cranial nerve

A 
1- cribiform plate 
2- optic canal 
3- SOF
4- SOF
5: V1- SOF
V2- foramen rotundum 
V3- foramen ovale 
6- SOF
7- IAM
8- IAM 
9- jugular foramen 
10-jugular foramen 
11- jugular foramen 
12- hypoglassal canal
255
Q

what is the motor supply of CNV3

A

muscles of mastication, tensor tympani and tensor veli palatini

256
Q

what is the motor supply of CN 7

A

muscles of facial expression (including orbicularis oculi for eye closure) and stapedius muscle.

257
Q

what is the sensory function of the facial nerve

A

part of the auricle

258
Q

what is the special sensory function of the facial nerve

A

taste to the anterior two-thirds of the tongue (chorda tympani).

259
Q

what is the parasymp function of the facial nerve

A

lacrimal gland (greater petrosal nerve) and submandibular/sublingual glands (chorda tympani).

260
Q

what are the functions of CN 9

A

Motor supply to stylopharyngeus
Parasympathetic supply to the parotid gland.
Sensory supply to the middle ear and the posterior third of the tongue.
Taste in the posterior third of the tongue

261
Q

what are the functions of the vagus nerve

A

Sensory supply to the external ear
Taste over epiglottis
Motor supply to the soft palate, larynx and pharynx.
Parasympathetic supply: bradycardia, peristalsis and vomiting.

262
Q

what muscles does the accessory nerve supply

A

SCM and trapezius

263
Q

what is the path of the pupillary light reflex

A

Light enters the eye causing signals to be sent along optic nerve. The signals exits the optic tract to the ipsilateral pretectal nucleus in the midbrain. The pretectal nuclei projects bilateral signals to both Edinger-Westphal nuclei.

Pre-ganglionic parasympathetic fibres, from Edinger-Westphal, travels along with the oculomotor nerve then exits to synapse with the post-ganglionic neurons in the ciliary ganglion. From the ciliary ganglion, the parasympathetic fibres are carried via the short ciliary nerves to innervate the ciliary muscle and sphincter pupillae (constrictor).

264
Q

what is accomodation

A

focusing on close objects

265
Q

what are the components of the accommodation reflex

A

Increase lens curvature: the ciliary muscle contracts (via parasympathetics form Edinger-Westphal) leading to relaxation of the suspensory ligaments of the lens.

Constriction of the pupils: activation of the sphincter pupillae (via parasympathetics form Edinger-Westphal).

Eye convergence: contraction of medial recti via cranial nerve III.

266
Q

what NT is released in both symp and parasymp ganglions to constrict or dilate the pupil

A

norepinephrine

267
Q

what is the pathway for pupil constriction

A

First order neurons: Start at the posterolateral hypothalamus and synapse at the intermediolateral cell column between C8 to T2.

Second order preganglionic neurons: leaves intermediolateral cell column, travels over lung apex and synapse at the superior cervical ganglion at the carotid bifurcation (where sudomotor fibres exits to course with the external carotid and supply the sweat glands of the face).

Third order postganglionic neurons: travels around the internal carotid artery to join the ophthalmic part of the trigeminal nerve. Then enters the ciliary ganglion (does not synapse) to supply the dilator pupillae via long ciliary nerves.

268
Q

what are the common signs of optic nerve dysfunction

A

Decrease in visual acuity (VA).
Dyschromatopsia: visual colour impairment (loose red first)
Visual field defects.
Diminished contrast sensitivity.
Relative afferent pupillary defect (RAPD).

269
Q

what can cause optic neuritis

A

infectious
demyelinating- MS (female predominance, 3rd/4th decade, more common further from equator), neuromyelitis optica (devic disease, bilateral ON, muscle weakness, increased tone and spasm)

270
Q

what are the clinical features of MS

A

sensory loss- numbness/ pins and needles
spinal cord symptoms (motor)- muscle cramping and weakness
autonomic features: bladder, bowel, sexual dysfunction
cerebellar: tremor, dysarthria, ataxia (charcots triad)
L’hermitte sign: electric shock on neck flexion
uhthoff phenomenon: worse symptoms due to increase in temperature

ophthalmic:
- ON: commonly presenting complaint, unilateral pain exacerbated by eye movements, decreased VA, central scotoma, dyschromatopsia, RAPD
- internuclear ophthamoplegia
- nystagmus

271
Q

what Ix for MS

A

demyelinating plaques on MRI

oligioclonal bands in CSF on LP

272
Q

what is the treatment for optic neuritis

A

IV methylprednisolone
then oral prednisolone
(treat MS)

273
Q

what is anterior ischaemic optic neuropathy (AION)

A

damage to the optic nerve due to ischaemia
can be non arteritic (caused by occulusion of short posterior ciliary artery- idiopathic, HTPx, diabetes, sleep apnoea) or arteritic (GCA causing occlusion of short posterior ciliary artery)

274
Q

what is the difference in presentations between arteritic and non arteritic AION

A

non arteritic:

  • > 50s
  • sudden vision loss
  • painless
  • unilateral
  • VA >6/60
  • inferior altitudinal visual field defect
  • sectoral hyperaemic disc swelling

arteritic

  • younger
  • sudden
  • painful
  • unilateral
  • severe visual loss
  • VA <6/60
  • scalp tenderness, headache, jaw claudication
  • chalk white diffue swollen disc
  • optic atrophy (pale disc)
275
Q

what type of AION causes more risk to the other eye

A

arteritic (90% is not treated) (GCA)

276
Q

what investigations for AION

A

arteritic :

  • ESR
  • CRP
  • temporal artery biopsy (sensitivity low due to skip lesions)

non arteritic:

  • BP
  • blood sugar
  • cup exam
  • exclude GCA
277
Q

Tx for AION

A

arteritic (GCA):
high dose IV methylprednisolone, then oral prednisolone + aspirin (if no CI)

non arteritic: treat cause

278
Q

what are the symptoms and signs of raised ICP

A

headache (worse in morning)
N/V
pulsatile tinnitus
deterioration of consciouness

279
Q

what are the signs and symptoms of papilloedema

A

symptoms of raised ICP
transient visual loss (lasts seconds)
enlarged blind spot
optic disc signs- hyperaemia, blurred margins of disc (early,
swelling and elevation of the whole optic disc, peripapillary splinter haemorrhages

280
Q

what is horners syndrome characterised by

A 
ptosis (muller muscle (superior tarsal muscle) dysfunction 
miosis 
ipsilateral anhydrosis (if lesion below superior cervical ganglion)
281
Q

what causes horners syndrome

A

lesion in the sympathetic pathway:

  • stroke, syringomyelia
  • pancoast tumour, carotid aneurysm/ dissection
  • ICA dissection, cluster HA, cavernous sinus lesion
  • trauma (most common in children)
282
Q

what does a painful horners syndrome make you think

A

carotid/ internal carotid artery dissection

283
Q

what Ix for horners

A

Apraclonidine can be used to confirm a Horner’s pupil: topical apraclonidine is an alpha-1 receptor agonist which causes pupillary dilation in the Horner’s pupil due to denervation hypersensitivity, however, normal pupil remain unaffected.
CT or MRI are used to identify tumours or artery dissection/aneurysm

284
Q

what is laternal medullary syndrome (wallenbergs syndrome)

A

occurs due to ischaemia to the lateral part of the medulla oblongata due to blockage of the posterior inferior cerebellar artery or vertebral artery:

  • Damage to the vestibular nucleus causing vertigo,vomiting and nystagmus.
  • Damage to the descending sympathetic system causing ipsilateral Horner’s syndrome.
  • Damage to the spinal trigeminal tract causing ipsilateral loss of pain/temperature and loss of corneal reflex.
  • Damage to the spinothlalamic tract causing contralateral loss of pain/temperature in the trunk and limbs.
  • Other symptoms include dysphagia and horseness.
285
Q

what is adies pupil

A

caused by loss of postganglionic parasympathetic innervation to the iris sphincter and ciliary muscle
-more common in females
- usually unilateral
- affected pupil is large
- blurring on near vision (slow constriction on accommodation)
Ix
Slit lamp
0.125% (low dose) of topical pilocarpine into both eyes. Adie’s pupil constricts (due to denervation hypersensitivity) while normal pupil doesn’t

286
Q

what is holmes adie syndrome

A 
diminished/ absent deep tendon reflex of lower limbs 
\+ 
adies pupil 
\+/-
orthostatic hypertension
287
Q

what is argyll robertson pupil

A

caused by diabetes (used to be neurosyphilis)

  • characterised by bilateral irregular small pupils
  • both pupils accommodate but do not react ;)
  • 0.1% pilocarpine does not cause constriction (opposite of adies)
288
Q

what do craniopharyngiomas cause

A

bitemporal haemianopias

can cause growth failure, delayed puberty, headaches, diabetes insipidus, obesity and hypothyroidism in children

289
Q

what visual defect do lesions in the optic tract cause

A

contralateral homonymous hemianopia

290
Q

what visual defect do lesions in the optic radiations cause

A

Temporal radiations:
Contralateral superior homonymous quadrantanopia “pie in sky”.
Parietal radiations:
Contralateral inferior homonymous quadrantanopia ”pie in floor”.
Main radiations:
Contralateral homonymous hemianopia.

291
Q

what visual defect do lesions in the occipital cortex cause

A

Occlusion of the calcarine artery of the posterior cerebral artery= Contralateral homonymous hemianopia with macular-sparing.

Damage to the tip of the occipital cortex in a posterior head injury= Congruous homonymous macular defects

292
Q

what are the signs and causes of a 3rd nerve palsy

A
  • ptosis
  • abduction and depression in primary position (down and out) with ophthalmoplegia
  • only abduction of eye is normal
  • dilated pupil
  • accommodation abnormality

causes: diabetes, HPTx (both microvascular) - are pupil sparing as blood supply to pupil no affected
posterior communicating artery aneurysm (acute painful), trauma, uncal herniation

293
Q

what syndrome present with 3rd nerve palsy

A

webers- stroke affevting ventral midrain: ipsilateral 3rd NP, contralateral hemiparesis (cerebral peduncle)

benedikts- stroke affecting dorsal midbrain, ipsilateral 3rd nerve palsy, contralateral tremor, ataxia, choea (red nucleus)

294
Q

what are the features and causes of a fourth nerve palsy

A

Vertical diplopia: worse on walking downstairs or looking down.
Hypertropia: the affected eye is higher than the contralateral eye. It is made worse on tilting the head to the ipsilateral shoulder.
Depression of the eye is limited: most noted on adduction. (SO innervated by CN4- cant look down and out)
Compensatory head tilt: to avoid diplopia, the patients tend to develop a contralateral head tilt.

most common causes: trauma, congenital (can get idiopathic or microvascular)- longst course through skull

295
Q

what are the features and causes of a 6th nerve palsy

A

Horizontal double vision: worse on looking at distant targets.
Esotropia in primary position.
Abduction is limited.

causes: microvascular: diabetes, HPTx
raised ICP (herniation of brain stem can stretch CN 6)
296
Q

what is myasthenia gravis

A

autoimmune disease of acetylecholine receptors at post synaptic NMJ
presents in 3rd decade of life
female predominance
affects voluntary muscles and smaller muscles first
occular involvement v high- presenting features

297
Q

what are the clinical features of MG

A

Ptosis: typically bilateral (can be unilateral initially) and worse at end of the day/prolonged upgaze.

Cogan lid twitch: brief upshoot of the lid elicited by making patient look downwards then upwards.
Diplopia.
Ophthalmoplegia.
Fragility and weakness of muscles of facial expression and proximal limb muscles.

298
Q

what Ix for MG

A

Ice test: ptosis improve after applying ice for 2 mins.
Antibodies: anti-ACh Receptor Antibody and anti-Muscle-Specific Kinase (MUSK) Antibody (can be positive in those with –ve anti-AChR).
Electromyograhy and muscle biopsy.
Imaging of thorax: can reveal thymoma as it can be associated with myasthenia.

299
Q

what treatment for MG

A

Pyridostigmine (anticholinesterase), steroids and immunomodulators.
Surgery if thymoma is present (thymectomy).

300
Q

what are the features of myotonic dystrophy

A

delayed muscular contraction and muscle wasting
Early onset cataract: iridescent dust like opacities on the lens resembling Christmas tree catarct.
Ptosis.
Hypermetropia.
Ophthalmoplegia.

301
Q

what causes myotonic dystrophy

A

autosomal dominant condition due to tri-nucleotide repeat on chromosome 19

302
Q

what causes NF 1 and NF2

A

mutation in the NF1 gene (chromosome 17)- autosomal dominant

NF2 gene (chromosome 22)

303
Q

what are the clinical features of NF1

A

Neurofibromas.
Café-au-lait spots: brownish spots most commonly in the trunk.
Axillary freckling.
Ophthalmic features:
Optic nerve glioma
Bilateral Lisch nodules: hamartomas pigmented lesions protruding above the iris.
Plexiform neurofibromas of the eyelid: “bag of worm” sensation.

304
Q

what are the clinical features of NF2

A

Cataracts.

Bilateral/unilateral acoustic neuromas: decreased hearing or tinnitus

305
Q

what is benign essential blepharospasm

A

A bilateral idiopathic condition characterized by involuntary contraction of the orbicularis oculi muscle. Typically presents in the sixth decade of life with a female predominance
treated with botox and artificial tears

306
Q

what does the cavernous sinus contain

A

within lateral wall- CN 3,4,5 (V1 and 2)

going through sinus= ICA (with sympathetic system) and CN 6

307
Q

where is the cavernous sinus

A

lateral to sella turcica

posterior to superior orbital fissure

308
Q

what can cause cavernous sinus syndrome

A

infections, tumours, cavernous sinus thrombosis, internal carotid aneurysm and carotid-cavernous fistula

309
Q

what are the features of cavernous sinus syndrome

A

Ptosis and ophthalmoplegia: due to compression of cranial nerves 3,4 and 6
Loss of corneal reflex: due to cranial nerve 5 (V1) involvement
Maxillary sensory loss: due to cranial nerve 5 (V2) involvement
Horner’s syndrome: due to involvement of internal carotid ocular sympathetics
Proptosis and periorbital swelling: due to increased venous pressure in the veins draining the orbit

310
Q

explain decoritate posturing and what it means

A

indicates severe brain damage to areas including the cerebrum, internal capsule and thalamus. The midbrain is generally spared. The patient presents with abnormal flexion of his arms, the hands are clenched into fists, and the legs extended and feet turned inward. This is because the lateral corticospinal tracts are disrupted so the rubrospinal tracts takes over causing the abnormal flexion to the upper extremities and the reticulospinal tracts takes over causing the extension of the legs.

311
Q

explain decerebrate posturing and what it means

A

indicates an even more severe brain damage and brainstem damage, specifically at a level below the red nucleus in the midbrain. The patient presents with his head arched back and both arms and legs extended. In this case, both the lateral cortical spinal tract and rubrospinal tract are damage so the reticulospinal tract takes over and causes extension of the whole body.

312
Q

what is the most significant section of the GCS

A

motor- drops only when there is a significant neurological issue

313
Q

what is the total volume of csf and how much is produced daily

A

total= 150ml

produced/ day = 450 ml

314
Q

what is the path of CSF

A

flows from the lateral ventricles to the third ventricle via the foramen of Munro (intraventricular foramen). From the third ventricle, the CSF flows through the (cerebral) aqueduct of sylvius to reach the fourth ventricle. The CSF then circulates back to the subarachnoid space through foramina of Magendie and Luschka and is absorbed by the arachnoid granulations back to venous blood

315
Q

what is the normal ICP range when supine

A

5-15 mmHg

316
Q

what happens to cerebral blood flow and prefusion pressure when ICP rises

A

both drop - can develop to ischaemia, brain swelling and herniation

317
Q

what is cushings triad of raised ICP

A

hypertension
bradycardia
irregular, decreased respiration

318
Q

what is an uncal herniation

A

medial temporal lobe herniating through tentorium

319
Q

what are the symptoms of an uncal herniation

A

The first symptom is pupillary dilatation due to involvement of the ipsilateral oculomotor nerve.
The herniated uncus further compresses the pyramidal tracts at the crus cerebri, causing contralateral hemiparesis.

320
Q

what is a subfalcine herniation

A

herniation of the cingulate gyrus below the falx cerebri

321
Q

what can a subfalcaine herniation cause

A

compression of the ipsilateral anterior cerebral artery, causing weakness in lower extremities

322
Q

what is a tonsilar herniation

A

displacement of the cerebellar tonsils into the foramen magnum

323
Q

what can cause a tonsilar herniation

A

a posterior fossa lesion or an Arnold-Chiari malformation

324
Q

what are the symptoms of a tonsilar hernation

A

medullary compression and ischaemia characterized by neck stinfness, abnormal neck posture, respiration anomaly (Cheyne-Stokes breathing; periods of tachypnea and tachycardia followed by periods of bradycardia and bradypnea) and coma.

325
Q

what can central herniation of the brainstem cause

A

diplopia due to sixth nerve palsy and brainstem dysfunction

326
Q

which layers of dura mater exist in the spine

A

only the meningeal (mot the periosteal)

327
Q

where are extra and epidural haematomas

A

between dura and skull

328
Q

what causes an extraudral haematoma

A

The separation of the dura from a bone following a shearing stress (head trauma) with the disruption of vessels causes the expansion of the haematoma.

The most common source of bleeding is from the disruption of the middle meningeal artery (the anterior branch of the middle meningeal artery is vulnerable to injury as it runs underneath the pterion) most commonly associated with a temporoparietal skull fracture.

The most common location for an EDH is the temporoparietal region but it can occur less commonly in the frontal, occipital or posterior fossa regions.

329
Q

what are the symptoms of an extradural haematoma

A

young adult sustaining a closed head trauma. The classic symptoms include a brief loss of consciousness, followed by a period in which the patient regains consciousness and awareness (called a lucid interval), after that the patients further deteriorates, exhibiting symptoms such as: headache, vomiting, contralateral hemiparesis (due to compression of the cerebral peduncle) and ipsilateral pupillary dilatation (the expanding haematoma causes the uncus of the temporal lobe to herniate and compress on the pupillary fibres of the oculomotor nerve).

Unlike subdural haematomas, the rapidity of the decline occurs as the expanding haematoma are from a high pressure arterial source, rather than from the low pressure venous system

330
Q

what Ix for extradural haematomas

A

CT

will see lens (lemon) shaped haematoma +/- mass effect/ herniation

331
Q

why is an extradural haematoma lens/ lemon shaped

A

as periosteal dura stuck to bone, blood can get over sutures

332
Q

Tx for extradural haematomas

A

for expanding extradural hematomas is immediate neurosurgical evacuation of the haematoma if there is significant or ongoing neurological deficit.
Conservative management is sometimes considered in neurologically intact patients with a small extradural haematoma.

333
Q

what is the presentation of a subdural haematoma

A

usually trauma
Most SDHs presents unilaterally in adults. However, bilateral SDHs are more common in children owing to the absence of adhesions in the subdural space which develop with ageing.

Acute SDH forms quickly and the patient becomes symptomatic immediately= severely decreased state of consciousness. Some patients can still remain conscious until the haematoma expands more and then deteriorate.

Chronic SDH, on the other hand, takes a longer time course, with a mean of 3-7 weeks before symptoms starts to present= headache and confusion. Other symptoms include: urinary incontinence, weakness, seizures, cognitive dysfunctions and gait abnormalities

334
Q

what is the pathophysiology of acute SDH

A

The acceleration/deceleration mechanism the brain is subjected to after a high impact trauma to the head, results in the rupturing of bridging veins (veins that drain the cotex and empty in dural sinuses). Cerebral blood flow can also be reduced and the blood volume in the brain decreases as a result from compression with midline shift and cerebral oedema due to increased Intracranial pressure

335
Q

what is the pathophysiolgy of a chornic SDH

A

brain atrophy main driving factor- due to age, chronic alcoholism or dementia (bridging veins are stretched and even minor trauma can cause them to rupture)
The leaky vessels result in the accumulation of blood in the subdural space and an osmotic gradient can form which draws more fluid in that space. The ICP then rises dramatically causing a decreased blood perfusion in the brain thus, the patient becomes symptomatic
Other predisposing factors is the use of anticoagulation, such as aspirin, which causes continued and non-stopped bleeding into the subdural space
or due to inflammationand angiogenesis- Following a traumatic head injury, inflammatory cells are recruited forming new membranes and activate inflammation. Angiogenesis also causes the formation of fragile leaky vessels within the membrane causing more blood and fluid accumulation

336
Q

what imaging for a SDHaematoma

A

CT
acute SDH- cresent shaped hypersensity
chronic SDH- hypOdense cresent shape

337
Q

what is normal pressure hydrocephalus

A

the buildup of CSF due to impaired resorption at the arachnoid granulations/ overproduction of CSF
mostly idiopathic, can be caused by trauma, meningitis or SAH

increased CSF but CSF pressure within normal range (does fluctauate and have nocturnal peaks)

338
Q

what does LP show in normal pressure hydrocephalus

A

normal opening pressure

339
Q

what are the clinical features of normal pressure hydrocephalus

A

apraxia of gait (commonly presenting symptom) = shuffling gait
dementia (can be reversible)
urinary incontinence (over activity of detrusor muscle due to reduced/ asbent central inhibition)

340
Q

what will be seen on imaging in normal pressure hydrocephalus

A

enlarged ventricles

341
Q

what is the treatment for normal pressure hydrocephalus

A

ventriculo-peritoneal shunt (reserved for patients with marked ventriculomegaly with severe symptoms/ marked improvement after removal of CSF)

342
Q

what is hydrocephalus

A

excessive accumulation of CSF leading to enlarged ventricles

343
Q

what are the types of hydrocephalus

A

communicating or non communicating:

  • communicating= no obstruction of flow between ventricles and sub arachnoid space. reduced absorption due to impaired arachnoid granulations
  • non communicating= obstruction in ventricular system (can usually tell by seeing if 4th ventricle small or not- if small NC) caused by tumour, colloid cyst (3rd ventricle), stenosis of aqueducts

congenital or acquired:
congenital= aqueductal stenosis (most common), type 2 arnold chiari malformations, spina bifida, dandy walker syndrome
- acquired= tumours, infections, trauma

344
Q

what are the symptoms of congenital hydrocephalus

A

failure to thrive
dilated scalp veins
increased head circumference
impaired upgaze due to compression on tectal plate
setting sun sign (downward deviation of the globe on lid retraction)
raised ICP and diplopia (6th nerve palsy)
vomiting
macewan sign ‘cracked pot’ sound on head percussion

345
Q

what are the symptoms of acquired hydrocephalus

A 
HA- worse in mornings 
vomiting 
diplopia
impaires upgaze
raised ICP
papilloedema 
drowsiness 
incontinence 
gait abnormalities
346
Q

Ix for hydrocepahlus

A 
congenital:
full obstetric and post natal Hx
head circumference 
fullness of ant fontanelle 
dilated scalp veins? 
ophthalmic evaluation

MRI best to find cause and site of obstruction
CT used in acute setting

347
Q

management for hydrocephalus

A

venticulomegaly + raised ICP= need CSF diversion asap

  • VP shunt (allows CSF to be absorbed outside CNS)
  • endoscopic 3rd ventriculostomy (creates direct pathway from 3rd V to basal cisterns + SAS- only works in non communicating as needs working absorption)
348
Q

what are chiari malformations

A

congenital/ acquired malformations of the hindbrain - affects cerebellum, medulla and upper cervical spinal cord structural relationships = causes impaired SF circulation through the foramen magnum

349
Q

what is a chiari I malformation

A

(most common + least severe)

  • caudal displacement of the cerebellar tonsils below FM
  • may be associated syringomyelia (expanding cystic cavity or syrinx in spinal cord that damages it)

causes HA (worse when coughing) with suboccipital pain (can be brought on by neck extension)
downbeat nystagmus
central cord symptoms (due to syringomyelia) - cape like sensory loss of temp and pain, progressive spastic paralysis starting with upper extremities
ataxic gait

350
Q

what is a chiari II malformation

A

(less common more severe)
happens more in children
caudal displacement of cerbellum AND medulla below FM with herniation of the 4th ventricle

associated with spina bifida
hydrocephalus and syringomyelia also common
patients present in infancy/ childhood:
-severe brain stem dysfunction in infants- dysphagia, apnoea, stridor, nystagmus
-weakness that may progress to quadriplegia

351
Q

management of chiari malformations

A

surgical or conservative

Suboccipital craniectomy and upper cervical laminectomy to decompress the malformation at the foramen magnum are usually required with cord drainage

aims to restore flow of spinal fluid

352
Q

what is pseudo tumour cerebri/ benign intracranial hypertension

A

idiopathic intracranial hypertension
(idiopathic disease that occurs when there is raised intracranial pressure with the absence of any space-occupying lesions or hydrocephalus. It occurs at a higher incidence in young females and obese patients)

353
Q

what are the clinical features of IIH

A

Headache: throbbing type which is worst first thing in the morning and is relieved on standing.
Moderate or gross bilateral papilloedema.
Nausea and vomiting.
Less commonly, sixth nerve palsy can occur due to increased intracranial pressure.

354
Q

what Ix for IIH

A

CT or MRI: shows a normal or reduced size of ventricles (“slit-like” ventricles).
Visual field testing and fundoycopic examination for papilloedema.
Lumbar puncture, if not contra-indicated.

355
Q

what is the management for IIH

A

initially medical with weight loss (if obese) and diuretics, such as acetazolamide, to help reduce the intracranial pressure.

Surgical intervention include CSF diversion techniques such as a lumbo-peritoneal shunt.

356
Q

Which one of the following is NHS standard of care for a symptomatic, easily accessible glioblastoma in a young, fit patient?

  1. Biopsy only
  2. Radiotherapy only
  3. Temozolomide chemotherapy only
  4. Maximal surgical debulking surgery only
  5. 2+3
  6. 2+3+4
A

6- radio, chemo and maximal surgical debulking

357
Q

A 6-month-old girl presented with a head circumference rising from the 66th to the 99th percentile and failure to thrive. On examination, when the lids are retracted, the eyes look like they are sunsetting, and upward gaze is impaired.

a) Non-communicating hydrocephalus due to arnold-chiari
b) Non-communicating hydrocephalus due to aqueduct stenosis
c) Communicating hydrocephalus due to arachnoid granulation dysfunction
d) Communicating hydrocephalus due to a colloid cyst

A

Non communicating (Most common cause of this is aqueduct stenosis)

358
Q

A 75 year old patient presents with a progressive shuffling gait and urinary incontinence. He denies any back pain. His wife is claiming that he has been forgetting his keys and taking his medication. What is the most likely diagnosis?

a) Chronic subdural haematoma
b) Cauda equina syndrome
c) Normal pressure hydrocephalus
d) Ischaemic stroke

A

normal pressure hydrocephalus

gait disturbance, ataxia, dementia, urinary incontinence presenting acutely in the elderly

359
Q

Dx:
A 56-year-old man presents with a headache, severity 8/10 with associated nausea. On examination he has ptosis, and miosis.

A

internal carotid dissection (causing horners syndrome)

360
Q

Dx:
A 56-year-old man presents with a progressive headache, severity 6/10 with associated nausea. On examination he has ptosis, and a right dilated unreactive eye

A

posterior communicating aneurysm (causing a 3rd nerve palsy)

361
Q

Dx:
A 56-year-old man presents with a headache, severity 10/10 with associated vomiting. On examination he has neck stiffness and photophobia

A

SAH

362
Q

A 40-year-old obese lady on the contraceptive pill develops headaches first thing in the morning which are worse on coughing. She is complaining of double vision. What could be causing her diplopia?

A

6th nerve palsy- causes: microvascular: diabetes, HPTx

raised ICP

363
Q

A 55 year old man develops diplopia after a closed head injury accident. He says the diplopia is worse when he is going down the stairs. On examination, you see he has a head tilt to the right.

A

4th nerve palsy- trauma

364
Q

A patient develops retro-orbital pain in his right eye described as a boring, worst pain he has ever felt, lasting 20 minutes. Associated tearing of that eye and a stuffy nose. He has 10 episodes of this pain for the past week.

A

cluster HA

365
Q

A 30-year-old female presented with double vision and ataxia. Three years earlier she had an episode where she lost vision in her left eye for two weeks. On exam, she was mildly ataxic, with brisk reflexes, and both horizontal and vertical nystagmus. What is the most likely diagnosis?

A

MS

366
Q

calculate the GCS score:
A 25-year-old man developed a severe headache and collapsed. Upon calling his name, he does not respond nor opens his eyes. However, when a painful stimulus is applied he internally rotates his shoulders and flexes his forearm and wrists while extending his legs

A

5

367
Q

Calculate the GCS score:
A 70-year-old woman presents with a headache and confusion, 4 weeks after she suffered from a fall. She opens her eyes spontaneously and moves her arms and legs when told to

A

14

368
Q

Calculate the GCS score:
A 20-year-old male presented to A&E after being in a car accident. Neurologic evaluation was as follows: he opened his eyes only to the sound of his name, he was able to localize to a painful stimulus but failed to move his arms and legs to command only. When asked where he was his reply was “my house to go”

A

11

Neurology (35 decks)

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