AAW - Neuro Flashcards
atrophy of caudate nucleus
huntington’s disease
depigmentation within the substantia nigra pars compacta
parkinson’s
symmetric lesions in the paraventricular regions of the thalamus and hypothalamus, mammillary bodies, and periaqueductal region of the midbrain
wernicke’s and korsakoff’s
neurofibrillary tangles
think:
think alzheimer’s
places in the brain not protected by the BBB
OVLT (organum vasculosum of the lamina terminalis; senses change in
osmolarity), area postrema - in the floor of the fourth ventricle (responds to emetics)
which area of the brain makes:
ADH
oxytocin
ADH: supraoptic nucleus
oxytocin: paraventricular nucleus
part of the hypothalamus responsible for:
hunger satiety cooling off/parasympathetic heating up/sympathetic circadian rhythm
hunger - lateral - zap the lateral and you shrink laterally
satiety - ventromedial - zap the ventromedial and you grow medially and ventrally
cooling - anterior hypothalamus - A/C = anterior cooling
heating - posterior - heated seats heat your posterior
circadian rhythm - suprachiasmatic nucleus - you need sleep to be charismatic (SCN –> NE release –> pineal gland –> melatonin)
part of the brain responsible for REM eye movement
PPRF paramedian pontine reticular formation
if you have a lesion here, your eyes look away from the side of the lesion
desmopressin acetate
mimics ADH, used to treat betwetting
preferred over imipramine because of the SE
mneumonic for stages of sleep
BATS Drink Blood
awake - beta awake (eyes closed) - alpha N1 - theta N2 - sleep spindles and K complexes N3 - Delta
REM - beta
thalamus nuclei
input from what nerve?
what sense is it?
VPL
VPM
LGN
MGN
The role of the thalamus is the major relay for all ascending sensory information except olfaction
VPL - ventral posteriolateral - input is spinothalamic and dorsal columns/medial lemniscus - pain and temp, pressure, touch, vibration, and proprioception - goes to the primary somatosensory cortex
VPM - ventral posteriomedial - trigeminal and gustatory pathway - face sensation and taste - goes to primary somatosensory cortex (put Makeup on your face)
LGN - Lateral geniculate nucleus - from CN II - does vision - goes to the calcarine sulcus - Lateral = Light
MGN - medial geniculate nucleus - from the superior olive and inferior colliculus of tectum - does hearing - goes to auditory cortex of temporal lobe - Medial = Music
VL - ventrolateral - from basal ganglia, cerebellum, does motor stuff
what do you get form lateral lesions in the cerebellum
medial lesions?
lateral lesions - voluntary movement of the extremities; when injured, get a propensity to fall toward injured (ipsilateral) side
levels of what change in the brain of someone with huntingtons
Caudate loses ACh and GABA
CAG repeat disease
sudden, wild failing of 1 arm
what is it called
where is the lesion
hemiballismus (“half of body ballistic”)
lesion is contralateral subthalamic nucleus (lacunar stroke - often from uncontrolled hypertension)
athetosis
slow, writhing movements; especially seen in fingers
lesion in basal ganglia (huntingtons)
primidone
used to treat essential tremor
when do you get a slow, zigzag motion when pointing/extending toward a target
cerebellar dysfunction (intention tremor)
patient has agraphia, acalculia, finger agnosia, and left-right disorientation
what happened
left parietal-temporal cortex (visual association cortex aka the angular gyrus)
Gerstmann syndrome
someone is in a coma
what part of their brain lesion specifically is responsible for reduced levels of arousal and wakefulness
reticular activating system (midbrain)
confusion, ophthalmoplegia, ataxia, memory loss,
wernicke-korsakoff syndrome
B1 (thiamine) deficiency and excessive EtOH
can be precipitated with sugar in the absence of B1
inability to make new memories
where in the brain is lesioned
anteriograde amnesia - hippocampus
an elepheant never forgets
but
a hippo makes new memories
where are your lesions if the eyes look
towards the lesion?
away from it?
towards a frontal eye field lesion
away from a paramedian pontine reticular formation lesion (abducens nerve)
from hi to low and low to hi correcting sodium mneumonic
“From low to high, your pons will die”
(Central pontine myelinolysis)
“From high to low, your brain will blow”
(cerebral edema/herniation)
Lewy bodies composed of alpha-synuclein - intracellular eosinophilic inclusion
parkinsons
damage in the brain in severe hypotension - Sx
upper leg/arm wea
MCA (Middle cerebral artery) stroke Sx
(effects temporal areas and posterior frontal area)
Sx: contralateral paralysis - upper limb and face
Contralateral loss of sensation - upper and lower limbs and face
Aphasia if in dominant (left) hemisphere
Hemineglect if lesion affects non dominant (usually right) side
ACA (anterior cerebral artery) stroke Sx
contralateral paralysis of lower limb
contralateral loss of sensation of lower limb
lenticulostriate artery stroke Sx, cause, area of damage
contralateral hemiparesis
caused by unmanaged hypertension (lacunar infarct)
lesion in the striatum, internal capsule
Deviation of the tounge to the right
limb weakness on the on the left
loss of discriminative tough, proprioception, and vibration sense on the left
where is the infarct
right anterior spinal artery
this is called medial medullary syndrome
(hypoglossal nerves don’t cross over)
medullary pyramid and corticospinal fibers of the pyramidal tract damage causes weakness
medial lemniscus is responsible for loss of discriminative touch, proprioception, and vibration sense
Vomiting, vertigo, nystagmus, decreased pain and temp sensation from ipsilateral face and contralateral body; dysphagia, hoarsness, decresed gag reflex, ipsilateral horner syndrome, ataxia, dysmetria
where is the stroke/lesion
PICA
lateral medullary syndrome (wallenberg)
Nucleus ambiguus effects are specific to PICA lesions “don’t PICA horse (hoarse) that can’t eat (dysphagia)”
vomiting, vertigo, nystagmus, paralysis of face, decreased lacrimation, salivation, decreased taste from anterior 2/3, decreased corneal reflex. decreased pain and temp sensation, decreased ipsilateral hearing, ipsilateral horners
lateral pontine syndrome
facial nucleus effects are specific to AICA lesions “facial droop means the AICA’s pooped)
locked in syndrome
stroke locations
basilar artery
pons, medulla, lower midbrain, corticospinal and corticobulbar tracts, ocular cranial nerve nuclei, paramedian pontine reticular formation.
eye is down and out, with ptosis and pupil dilation
what artery
posterior communicating artery
lesions are typically aneurysms, not strokes.`
“worst headache of life”
rupture of a berry aneurysm leads to subarachnoid hemorrhage
epidural hematoma rupture of what artery
rupture of middle meningeal artery (branch of maxillary artery) often secondary to fracture of temporal bone
lucid period
LMN neuron lesion with flaccid paralysis
what part of the spinal cord was damaged
destruction of the anterior horns
get poliomyelitis and spinal muscular atrophy (werdnig-hoffmann disease)
enzyme deficit you might see in ALS
defect in superoxide dismutase 1
cause of tabes dorsalis. Sx?
tertiary syphilis. Results from degeneration (demyelination) of dorsal columns and roots
impaired sensation and proprioception and progressive sensory ataxia (inability to sense or feel the legs –> poor coordination)
syringomyelia - lesion region
anterior white commissure of the spinothalamic tract (second order neurons)
get bilateral loss of pain and temperature sensation, seen with Chiari I malformation; can expand and affect other tracts
what causes subacute combined degeneration of the spinal cord
vitamin B12 or vitamin E deficiency
get demyelination of dorsal column, lateral corticospinal tracts, and spinocerebellar tracts; ataxic gait, parasthesia, impaired position and vibration sense
blown pupil
what arteries could the stroke have occurred in
posterior cerebral
superior cerebellar
(cranial nerve III exists the midbrain between these two arteries)
patient has “lateral gaze palsy” or “nystagmus on lateral gaze” where is the lesion (nucleus and artery)
in CNVI (abducens) in the middle of the pons pontine branches of the basilar artery
mneumonic for reflex origins in the spinal cord
S1, 2—“buckle my shoe” (Achilles reflex)
L3, 4—“kick the door” (patellar reflex)
C5, 6—“pick up sticks” (biceps reflex)
C7, 8—“lay them straight” (triceps reflex)
inability to look up
where is the lesion
parinaud syndrome
paralysis of conjugate vertical gaze due to lesion in the superior colliculi of the brain stem (your eyes are above your ears, and the superior colliculus (visual) is above the inferior colliculus (auditory) (can be caused by a pinealoma)
nerve that innervates the superior oblique
trochlear (CN IV)
function of nucleus solitarius
Visceral sensory information (taste, baroreceptors, gut distention)
its a vagal nucleus
gets inputs from facial, hypoglossal, and well as the vagus
function of the nucleus ambiguus
motor innervation of pharynx, larynx, and upper esophagus (swallowing, palate elevation)
it is a vagal nuclei, but also gets inputs from IX, XI
dorsal motor nucleus
on of the vagal nuclei along with solitarius and ambiguus
sends autonomic (parasympathetic) fibers to the heart, lungs, upper GI
brain abnormality of autopsy of patau baby?
holoprosencephaly
what areas of the brain are effected during paralysis in a patient with central pontine myelinolysis
Corticobulbar - muscles of the face, head, neck
Corticospinal - torso, upper and lower limbs
lesions in medial longitudinal fasciculus cause what
often seen in what disease
The lesion causes Internuclear ophthalmoplegia
the MLF coordinates both eyes to move in the same horizontal direction. they are highly myelinated because then must communicate quickly so eyes can move at the same time.
lesions seen in people with demyelinating disease like MS
(MILFs (MLFs) get MS, and you gotta watch them walk by)
mech of succinyl choline
binds to ACh receptors irreversible for the first moments, but can be dissociated later.
used to paralyze people in surgery
reverse it with neostigmine later