Neuro- week 4 Flashcards

1
Q

Ischaemic stroke

A

an episode of neurological dysfunction caused by focal cerebral, spinal or retinal infarction

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2
Q

Silent CNS infarction

A

only visible through imaging or neuropathological evidence

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3
Q

Stroke caused by intracerebral hemorrhage

A

Rapidly developing clinical signs of neurological dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma.

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4
Q

Silent cerebral hemorrhage

A

A focal collection of chronic blood products within the brain parenchyma, subarachnoid space, or ventricular system on neuroimaging or neuropathological examination that is not caused by trauma and without a history of acute neurological dysfunction attributable to the lesion

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5
Q

Subarachnoid hemorrhage

A

Bleeding into the subarachnoid space (the space between the arachnoid membrane and the pia mater of the brain or spinal cord).

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6
Q

Stroke caused by subarachnoid hemorrhage

A

Rapidly developing signs of neurological dysfunction and/or headache because of bleeding into the subarachnoid space (the space between the arachnoid membrane and the pia mater of the brain or spinal cord), which is not caused by trauma.

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7
Q

Stroke caused by cerebral venous thrombosis

A

Infarction or hemorrhage in the brain, spinal cord, or retina because of thrombosis of a cerebral venous structure. Symptoms or signs caused by reversible edema without infarction or hemorrhage do not qualify as stroke.

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8
Q

Stroke, not otherwise specified

A

An episode of acute neurological dysfunction presumed to be caused by ischemia or hemorrhage, persisting ≥24 hours or until death, but without sufficient evidence to be classified as one of the above.

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9
Q

what is the global lifetime risk of stroke

A

25% and rising

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10
Q

what are the internal carotid arteries referred to as?

A

anterior circulation

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11
Q

what type of circulation are the vertebral arteries

A

posterior circulation

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12
Q

what percentage of patients do not have a complete circle of willis

A

50%

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13
Q

describe total anterior circulation stroke (TACS)

A

large cortical stroke

anterior or middle cerebral arteries

15% of strokes

symptoms
    unilateral weakness and/or sensory deficit of the 
    face and/or arms and/or legs
    homonymous heminopia
    higher cerebral dysfunction
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14
Q

describe partial anterior circulation stroke (PACS)

A

cortical stroke

anterior or middle cerebral arteries

35% of strokes

2/3 of the TACS criteria:
    unilateral weakness and/or sensory deficit of the 
    face and/or arms and/or legs
    homonymous heminopia
    higher cerebral dysfunction
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15
Q

lacunar stroke (LACS)

A

subcortical stroke

small deep perforating arteries

25% of all strokes

  1. pure motor, sensory or sensorimotor (Min 2; face, arm, leg)
  2. ataxic hemiparesis
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16
Q

posterior circulation stroke (POCS)

A

cortical, cerebellum, brainstem stroke

posterior cerebral artery, vertebral artery, basilar artery and branches

25%

  1. cerebellum or brainstem syndrome
  2. loss of consciousness
  3. isolated homonymous heminopia
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17
Q

define apraxia

A

Inability to perform purposeful movement despite motivation, and preserved overall neurological function – typically left hemisphere localization

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18
Q

define ‘Executive’ apraxias

A

Deficit in ‘sequencing’ complex movements - SMA & PMA in frontal cortex

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19
Q

define ‘Posterior’ apraxias

A

Deficit in the spatial construction of complex movements – posterior parietal cortex

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20
Q

describe whats involved in the corticospinal tracts and what does dysfunction cause

A

motor regions of cerebral cortex
brainstem
spinal cord
motor response

weakness and spasticity

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21
Q

describe whats involved in the basal ganglia loop and what does dysfunction cause

A

motor regions of cerebral cortex
thalamus
basal ganglia

movement disorder

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22
Q

describe whats involved in the cerebellar loop and what does dysfunction cause

A

motor regions of cerebral cortex
thalamus
cerebellum

coordination disorders

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23
Q

Spasticity – “clasp knife”

A
  • Pyramidal tract disorder – upper motor neurone
  • Most tone at beginning and end of range of movement
  • Deep tendon reflex primed to contract but usually you have descending inhibition from the cortex – problem with UMN leads to increase in these reflexes when stretch is max – beginning and end of range of movement
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24
Q

Rigidity

A
  • Extra-pyramidal – basal ganglia
  • Increased tone throughout movement
  • “lead pipe”
25
Q

Paratonia (you keep forgetting one thing)

A
  • Voluntary resistance
  • Executive system pathology
  • Typical seem in delirium/ dementia
26
Q

what are UMN lesion signs

A

spasticity
brisk reflexes
pyramidal pattern weakness (strong biceps and weak triceps (extensors). Opposite for legs where HAMS (flexors) are weaker than the quads

27
Q

what are extrapyramidal signs

A

rigidity
tremor
normal reflexes
no weakness

28
Q

describe parkinsons

A

A lack of dopamine supply to the basal ganglia - male 2:1 female
Alpha-synucleinopathy - build up of alpha synuclein
Bradykinesia
Rigidity
Tremor
Postural instability
+ ‘non-motor’ symptoms

Parkinson’s treatment includes giving L-DOPA and a DOPA decarboxylase inhibitor to make sure its only converted to dopamine in the CNS

29
Q

what are the pathways from the basal ganglia

A

Basal Ganglia structure receive signals from, and project to, the motor cortex

Direct pathway
The “accelerator”: pro-movement
D2 receptors for dopamine

Indirect pathway
The “brake”: anti-movement
D1 receptors for dopamine

30
Q

what are some jerky hyperkinetic disorders?

A

tremor

chorea

tics

31
Q

what are some non-jerky hyperkinetic disorders?

A

dystonia

myoclonus

stereotypies

32
Q

where do the spinal nerves pass out?

A

upper 7 cervical nerves pass through the intervertebra; foramen above the appropriate vertebra

Other spinal nerves pass through the intervertebral foramen below the appropriate vertebra. This results in there being 8 cervical spinal segments and nerves while there are 7 cervical vertebrae.

33
Q

what is the conus medullaris

A

the lower limit of nervous tissue

34
Q

what is the filum terminale

A

a cord of connective tissue connecting the conus medullaris and the 1st coccygeal vertebra

35
Q

what is caused by an upper spinal cord lesion

A
  • Spastic tetraplegia
  • hyperreflexia
  • extensor plantar responses
  • incontinence
  • sensory loss below lesion
  • Proprioception problems
36
Q

what is caused by a lower cervical cord lesion

A
  • UMN - lower limbs affected
  • LMN – upper limbs affected
  • Sensation affected
37
Q

what is caused by hemisection of the spinal cord

A

Brown-Séquard
• Ipsilateral loss of proprioception
• Contralateral loss of pain and temperature

38
Q

what does anterior spinal artery thrombosis cause

A

supplies 2/3 of the blood to the spinal cord – can cause damage to spinal cord – first LMN signs then UMN signs – preservation of proprioception

39
Q

describe brachial plexus lesions

A

• Traction lesions
o Upper roots (C5 & C6) – Erb’s palsy – “waiters tip”
o Lower roots (C8 & T1) – claw hand
• Neoplastic involvement
• Radio-therapy related

40
Q

describe radial nerve lesions

A
  • C6 – C8
  • Damaged by fractures to the mid shaft of the humerus
  • Compression at this site leads to “Saturday night paralysis” – loss of extension of wrist and fingers (wrist drop)
41
Q

describe median nerve lesions

A
  • C5-T1 (maintly C6)

* Carpal tunnel syndrome – predominantly sensory but there can be wasting of thenar muscles

42
Q

describe ulnar nerve lesions

A
  • C7, C8, T1
  • May be damaged at the medial epichondyle or at the medial aspect of the wrist.
  • Characteristic claw hand deformity
43
Q

describe femoral nerve lesions

A
  • L2 – L4
  • May be damaged by hip dislocation, pelvic fracture or tumours
  • Leads to weakness of knee extension (inability to lock knee while walking) and some wasting of quads
44
Q

describe sciatic nerve lesions

A

• L4-S3
• This is composed of two trunks which are bound together and separate in mid thigh
o Tibial nerve
o Peroneal nearve
• Damage can be due to trauma, neoplasm or operative complication

  • Much more common is compression or irritation of a spinal root which comprises the sciatic nerve (sciatica)
  • Symptoms dependant on the nerve root

• Common
o L5; sensory- pain in posterolateral thigh and leg, numb inner foot
 motor- weakness of dorsiflexing foot and toes
o S1; sensory- pain in posterolateral thigh and leg, numb lateral foot
 motor- weakness of foot dorsiflexion and loss of ankle jerk

• Rare
o L3+L4- diminished knee jerk, pain in anterior thigh

Sciatica can be caused by:
• Prolapsed intervertebral disk – typically posteriorly
o Can be treated by microdiscectomy to remove prolapsed material

45
Q

describe common peroneal nerve lesions

A
  • L4-S2
  • This can be damaged as the nerve winds round the head of the fibula. This can be a fracture or a tight cast
  • Results in weakness of foot dorsiflexion and eversion
46
Q

describe the occulomotor nerve

A

• Motor
• oculomotor nucleus in midbrain (LMN), innervates most extra-ocular muscles
• Parasympathetic motor
• arise from Edinger-Westphal nucleus in the
brainstem and pass to the ciliary ganglion.
Post-ganglionic fibres innervate the pupil
(constrict).

  • Damage results in the ipsilateral eye being deviated downward and laterally (“down and out”), ptosis, and a fixed dilated pupil.
  • May be damaged in raised intracranial pressure with tentorial herniation, or disorders involving the cavernous sinus.

Oculomotor nerve supplies all these muscles apart from the superior oblique and lateral rectus

47
Q

describe the trochlear nerve

A
  • Only cranial nerve to arise from the dorsal surface of the brainstem.
  • Motor
    * Supplies the superior oblique muscle

• Damage results in diplopia when looking downward and medially (direction globe moves when sup. oblique contracts).

48
Q

describe the abducens nerve

A

• Motor
– supplies the lateral rectus muscle.

• Damage results in diplopia when looking laterally.

49
Q

describe the trigeminal nerve

A

• Motor supply
– Supplies the skeletal muscles of mastication
which all develop from the first branchial arch.
Fibres arise from the trigeminal motor nucleus
and join the mandibular division of the
trigeminal nerve.
• Sensory supply
– the trigeminal ganglion is the equivalent
of a dorsal root ganglion and receives
sensory input from three branches;
ophthalmic, maxillary and mandibular.

There are three sensory nuclei;
• mesencephalic; proprioception from jaw
• chief sensory nucleus and spinal nucleus
– Fibres decussate and pass to thalamus.

50
Q

describe the facial nerve

A

• Motor
– supplies the muscles of facial expression
which develop from the second branchial
arch, and stapedius, stylohyoid and part of
digastric
• Parasympathetic motor
– pre-ganglionic fibres arise in the sup.
salivatory nucleus and pass to;
• pterygopalatine ganglion (lacrimal gland)
• submandibular ganglion (submandibular
and sublingual salivary glands)
• Sensory
– cutaneous sensory information from the
external ear. 1st order neurones lie in the
geniculate ganglion (middle ear) and axons
pass to the spinal trigeminal nucleus.
• Special sensory
– the chorda tympani nerve innervates (taste)
the anterior 2/3rds of the tongue. 1st order
neurones lie in the geniculate ganglion
(middle ear) and pass to the nucleus solitarius
(also receives fibres from IX and X).

• Conditions affecting VIIth nerve include;
– Bell’s palsy; unilateral facial paralysis
– Geniculate herpes zoster (vesicles in ear
drum)

  • UMN lesion- upper facial muscles are relatively well preserved due to bilateral innervation of the facial nucleus.
  • LMN lesion- paralysis of both upper and lower facial muscles.
51
Q

describe the vestibulocochlear nerve and some conditions that would affect it

A

• Special sensory
– sensory information relating to hearing
(cochlear nerve) and balance (vestibular
nerve). 1st order neurones in the vestibular
and cochlear ganglia pass to vestibular (4)
and cochlear nuclei (2) in the medulla.

• Symptoms of VIIIth nerve damage
– deafness, tinnitus
– dizziness, vertigo

• Conditions involving the VIIIth nerve include;
– Acoustic schwannoma
– labyrinthitis
– Meniere’s disease

52
Q

describe the glossopharyngeal nerve

A

• Motor
– fibres arise from the nucleus ambiguus and
innervate a single pharyngeal muscle which
arises from the third and fourth branchial
arches (stylopharyngeus).
• Parasympathetic motor
– fibres arise from the inf. salivatory nucleus
and pass to the otic ganglion, from where
post-ganglionic fibres innervate the parotid
gland.
• Sensory
– provides sensory information from the
pharynx, posterior 1/3rd of the tongue and the
middle ear. 1st order neurones lie in the
ganglion and pass to the trigeminal sensory
nucleus. Important in the gag reflex.
• Special sensory
– taste information passes from posterior 1/3rd
of the tongue and the pharynx to the nucleus
solitarius.
– information from the carotid body and carotid
sinus passes to the nucleus solitarius.

53
Q

describe the vagus nerve

A

• Motor
– fibres arise from the nucleus ambiguus and
innervate muscles of the soft palate, pharynx,
larynx and oesophagus which arises from the
third and fourth branchial arches . Important in
swallowing and speech.
• Parasympathetic motor (MAIN PARASYMPATHETIC
NERVE IN THE BODY)
– fibres arise from the dorsal motor nucleus
and pass to a number of ganglia within
the cardiovascular, respiratory and
gastrointestinal systems.
• Sensory
– provides sensory information from the
pharynx, larynx, tympanic membrane and part
of outer ear. 1st order neurones lie in the
ganglion and pass to the trigeminal sensory
nucleus. Important in the gag reflex.
• Special sensory
– Taste information passes from the pharynx to
the nucleus solitarius.
– information from the aortic body and aortic
arch passes to the nucleus solitarius.

54
Q

describe the accessory nerve

A

• Motor
– LMN’s are in the nucleus ambiguus and in the
anterior horn of the upper cervical cord. They
innervate trapezius and sternomastoid. (ask
patient to shrug shoulders)

55
Q

describe the hypoglossal nerve

A

• Motor
• This innervates both the extrinsic and
intrinsic muscles of the tongue. LMN’s are in
the hypoglossal nucleus.
• Unilateral lesions result in weakness and
atrophy of the tongue on the affected side.
When protruded the tongue deviates
towards the affected side.

56
Q

describe bulbar and pseudobulbar palsy

A

• Bulbar refers to the motor nuclei of the brainstem (strictly the medulla[“bulb”]). Corticobulbar fibres pass from the cortex to brainstem nuclei. As with elsewhere in the motor system there are UMN (pseudobulbar) and LMN (bulbar) lesions.
– Bulbar (LMN); atrophy and fasciculation
of the innervated muscles.
– Pseudobulbar (UMN); usually have to be
bilateral lesions due to bilateral
innervation. Exaggerated reflexes (jaw)
and spastic paresis of the tongue.
– Dysphonia, dysphagia and dysarthria are
seen in both.

  • Bulbar palsies are most commonly seen in MND (chronic) and Guillain-Barre (acute).
  • Pseudobulbar palsies are most commonly seen in vascular disease and demyelination.
57
Q

whats imprtant about the jugular foramen

A

The lower cranial nerves (IX, X, XI) may all be affected at the base of the skull (jugular foramen) by tumour, trauma or an inflammatory process. XII leaves the skull via the hypoglossal foramen and is only affected by large tumours.

58
Q

what is the reticular formation

A

Periaqueductal grey matter (midbrain) has ascending arousal pathways, and descending pain suppression pathways