Neurology PassMed Flashcards
Cranial nerve palsy responsible for ‘down and out’ motor deficit
Cranial nerve III
Key causes of cranial nerve III palsy
Posterior communicating artery aneurysms and diabetic ophthalmoplegia
- the differentiating feature between the two is that posterior communicating artery aneurysms present with pupillary dilation first (due to compression of peripheral parasympathetic fibres) whilst diabetic ophthalmoplegia present first with motor deficits (i.e. ‘down and out’ pupil)
Definition of a TIA
Updated guidelines: tissue based not time based
A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction
Mechanism of action: memantine
+ Use
NMDA antagonist
Use: second line treatment for Alzheimer’s disease
Example of acetylcholinesterase inhibitors
Donepezil
Rivastigmine
Galantamine
Thoracic outlet syndrome
Pathology: compression of the neurovascular bundle between the supraclavicular fossa and the axilla
Symptoms: nervous (90%), venous or arterial compression
Causes: congenital (e.g. presence of cervical rib), traumatic (e.g. following seatbelt trauma in car accident) or acquired (e.g. secondary to malignancy pressure effect).
Contralateral homonymous hemianopia with macular sparing and visual agnosia
posterior cerebral artery
Contralateral hemiparesis and sensory loss, lower extremity > upper
Anterior cerebral artery
Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia
Middle cerebral artery
Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity
Weber’s syndrome (branches of the posterior cerebral artery that supply the midbrain)
Ipsilateral: facial pain and temperature loss
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus
Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome)
Symptoms are similar to Wallenberg’s (see above), but:
Ipsilateral: facial paralysis and deafness
Anterior inferior cerebellar artery (lateral pontine syndrome)
‘Locked-in’ syndrome - artery?
Basilar artery
Lacunar strokes
present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
strong association with hypertension
common sites include the basal ganglia, thalamus and internal capsule
Why do nerve lacerations have worse recovery than nerve crush injuries
Nerve lacerations cause neurotmesis (damage to the axon, myelin sheath and surrounding connective tissue). This leads to degradation of the axon distal to the site of injury - this usually occurs within 1-2 days of the injury.
nerve crush injuries cause axonotmesis (disruption to the axon but there is preservation of the myelin sheath). This leads to an improved likelihood of healing, albeit a slow recovery process.