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Flashcards in week 3 Deck (40):

origin of the facial nerve

the pons. Begins as two roots (large motor and a small sensory)


greater petrosal nerve function

parasympathetic innervation of the lacrimal and mucous glands (excluding the parotid)


nerve to stapedius

stapedius muscle acts to stabilise the stapes, reducing the amplification of sounds


chorda tympani

provides special sensory fibres to the anterior two-thirds of the tongue, and some parasympathetic fibres to the submandibular and sublingual glands


where the facial nerve exits the cranium

stylomastoid foramen


origins of the vestibulocochlear nerve

vestibular component - vestibular nuclei located in the pons and medulla
Cochlear component - ventral and dorsal cochlear nuclei located in the inferior cerebellar penduncle


type of neurons in the vestibulocochlear nerve

bipolar - special sensory



beign cerebellopontine angle tumour that grows from the superior component of the vestibulocochlear nerve. Slow-growing tumour of the schwann cells which surround both the facial and vestibulocochlear nerve . Tumour normally arises from the vestibular branch


key defining symptom of a schwannoma

unilateral sensorineural hearing loss


menieres disease

auditory disease characterised by an episodic sudden onset of vertigo, low-frequency hearing loss, low frequency roaring tinnitus, and a sensation of fullness in the affected ear. Cause unknown but thought to be due to overproduction or impaired absorption of endolymph in the ear.


if there is an extra-cranial lesion to the facial nerve what type of functions will be damaged




Tarsorrhaphy is a surgical procedure in which the eyelids are partially sewn together to narrow the eyelid opening. It is done to ensure the cornea does not dry out, as patients may have weakness in their orbicularis oris muscle, meaning they cannot close their eye.


incomplete lesion

term used to describe partial damage to the spinal cord. Some motor and sensory function will remain. Depends on where the lesion has occurred in the spinal cord as to what functions remain (sensory and/or motor


first reflexes to return after spinal shock

babinski and bulbocavernous


Autonomic dysreflexia

• Spinal cord lesions above the T6 spinal cord level (generally)
• Acute AD is a reaction of the ANS to overstimulation
• Characterised by
o paroxysmal hypertension (the sudden onset of severe high blood pressure)
 throbbing headaches,
 profuse sweating,
 nasal stuffiness,
 flushing of the skin above the level of the lesion,
 slow heart rate, anxiety
• Believed to be triggered by afferent stimuli originating below the level of the spinal cord lesion
o Noxious stimuli
• Leads to sympathetic over-reaction
• Can be brought on by a blocked catheter


frontal lobe

movement, decision-making, problem solving and planning. Three main divisions:
prefrontal cortex - personality expression and planning of complex behaviours.
premotor cortex - voluntary muscle movement
primary motor cortex


parietal lobe

processing of tactile sensory information such as pressure, touch and pain. Location of the somatosensory cortex


occipital lobe

main centre for visual processing - location of the primary visual cortex


temporal lobe

structures of the limbic system are located here.
Lobes are involved in organising sensory input, auditory perception, language and speech production
Location of Wernicke's and Broca's areas, as well as the primary auditory cortex


Broca's area

motor aspects of speech - damage to this area will result in expressive aphasia, non-fluent and slow speech


Wernicke's area

sensory language understanding, and lexical processing. Damage to this are will result in receptive aphasia and extremely poor comprehension


primary auditory cortex

processing of sound information


corpus striatum

caudate nucleus, putamen and globus pallidus


subthalamic nuclei

produces the excitatory neurotransmitter glutamate


substantia nigra

production of dopamine, involved in the nigro-striatal pathway



located deep within the medial temporal lobes - primary role in the processing memory of emotional reactions



formation, organisation and storage of memories


Primary brain injury

occurs during the initial insult of a traumatic brain injury, resulting from the displacement of physical structures of the brain. Includes concussions



brain injury associated with a loss of consciousness, typically for a few minutes. There are no persisting abnormal neurological signs, although long-term symptoms such as a headache, impaired concentration etc. may be reported.


diffuse axonal injury

generally follows significant rotational acceleration and deceleration forces, causing widespread damage to axonal tracts. May be present without abnormal imaging findings but where there are MRI is best, and haemosiderin can be seen deposited at the junctions of deep grey and white matter, within white matter tracts, or in the basal ganglia.
Treatment is supportive. Injuries generally result in substantial cognitive impairment and personality change with/ or without physical neuro-disability.


results of raised ICP

can cause focal neurological deficit, dependent on the location of the bleed and where the pressure is being applied.
If untreated then coning can occur:
one or both temporal lobes can herniate through the tentorium cerebelli. This compresses the midbrain and third cranial nerve
herniation of the cerebellar tonsils through the foramen magnum, compressing the medulla. Can cause neurological deterioration and death


epidural haemorrhage

blood accumulation in the space between the dura and the calvarium. More common in young children than adults as their dura is less tightly attached to their skulls.
Usually occurs following a skull fracture in the temporal region - no primary brain injury usually.
Due to rupture of the middle meningeal artery (or a branch of this.) Results in an acute epidural haemorrhage, that if not stopped rapidly can lead to temporal lobe herniation and death.


subdural haematoma

usually a result of tearing of the cerebral veins due to some sort of injury. Leads to pooling of blood in the potential space between the dura and arachnoid mater. Forms slower due to the venous supply and generally occurs after some form of primary brain injury.
Acute subdural haematoma is more common in the elderly as the brain is more mobile in the cranial cavity


intracerebral haematoma/haemorrhage

can be single or multiple. More commonly occurs in the frontal or temporal lobes.
May occur in association with the severe motion that the brain undergoes during a head injury. Can occur as a result of a contusion coalescing into a haematoma.
temporal haematomas are more dangerous as the brain can herniate laterally (temporal lobe is liable to herniation)



a state of alertness and attentiveness to one's environment and situation. A fully conscious individual is awake, alert, orientated in time, person, place and current circumstance


cerebral perfusion pressure

the difference between mean arterial pressure and intracranial pressure. It represents he gradient that drives cerebral blood flow. Normally auto-regulated by the brain by altering the resistance of cerebral blood vessels.



intracranial haemorrhage affecting a brain lobe which is mixed with necrotic brain tissue which has ruptured into the subdural brain space


Key genes for eye development

PAX6 - master gene for eye development (activatory), restricted to optic cup and lens by PAX-2 which is present in the optic stalk and which is upregulated by SHH
SHH - orbit seperation


factors inhibiting neuronal regrowth in the CNS (recovery of function)

Neurons degenerate at a very slow rate (months to years)
Only grow small re-growths, then astrocyte hypertrophies, formation of a glial scar
Increased ECM molecule production by astrocytes and oligodendrocytes
Myelin (jettisoned by oligodendrocytes) and oligodendrocytes both contain anti-growth molecules


neural plasticity

the ability of the CNS to change it connectivity and can occur in various contexts including learning, memory, damage and learning