Learn neuro 2 week 2a (by zms21) – memorize.com – remember and understand brain anoxia

Edit basal ganglia – bishop 1 question


Role of basal ganglia

Initiating movement, regulates gain/velocity of cortical output, inhibitory output may selectively block competing motor programs to prevent them from interfering with voluntary movements from other CNS structures

Striatum composed of?

Caudate, putamen, nucleus accumbens

Output of basal ganglia?

Substantia nigra and globus pallidus interna

Caudate location?

In wall of lateral ventricle

Putamen vs. Caudate input?

Putamen involved in motor function via loops to ventrolateral thalamus/motor cortex, caudate involved in cognitive function via loops to dorsomedial thalamus and prefrontal cortex (more association areas)

Output of striatum?

INHIBITORY to target neurons

brain anoxia

Substantia nigra

=pars reticulata (large gabaergic neurons, eye movements) + pars compacta (cells here have neuromelanin and dopaminergic neurons affected in parkinsons)

Huntington’s disease

Loss of medium spiny neurons (in striatum) which are gabanergic+specific peptides, loss of enkephalin, neurons giving rise to indirect pathway are lostdecreased inhibition of gpeincreased inhibition of subthalamic neuronsreduces excitation of gpireduced inhibition of thalamusmore excitation in cortex

Output neurons of striatum

Medium spiny neurons express either D1 or D2- gabanergic + specific peptides (enkephalin or substance P + dynorphin)


Project to internal globus pallidus, excited/depolarized by dopamine, neurons containing substance P/dynorphin/GABA

brain anoxia


Project to external globus pallidus, inhibited by dopamine, neurons containing GABA/enkephalin

Edit basal ganglia – bishop 2 question


Globus pallidus external

Regulates output of gpi via connections with subthalamus and SN, INDIRECT pathway gabaergic, D2 receptors

Globus pallidus internal

Primary output of basal ganglia for limb movements, DIRECT pathway gabaergic, D1 receptors

Afferent projections to subthalamus?

From gpe is inhibitory, from cerebral cortex is excitatory

Efferent projections from subthalamus?

All excitatory to gpi/snr/gpe


Analogous to gpi (limb movements) but is primary output of basal ganglia for eye movements, large gabaergic neurons

Lenticular fasciculus

Axons coursing from gpi to thalamus

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Between thalamus and SN, glutamatergic neurons, only excitation source in BG


Dorsal to pars reticulate, has dopaminergic neurons

Pedunculopontine nuclei

Adjacent to superior cerebella peduncle in pontine reticular formation, projects to motor centers in brainstemcord, link between BG and motor neurons

Direct loop

Excitatory projection as motor regions of cortexputamen to neurons with D1 receptor gpi/snr to thalamus which is an inhibitory projection, **disinhibition (excitation) of thalamus and motor cortex

Indirect loop

Cortexstriatum to neurons with D2 receptor  gpe (suppressed so less inhibition of subthalamus) subthalamus (stronger output to gpi) snr/gpi thalamus (increased inhibition in thalamus)cortex (decreased excitation or disfacilitation in cortex )

brain anoxia

Edit basal ganglia – bishop 3 question


Tonic activity

Putamen has low levels, gpe/gpi/snpr have high levels


Removal of excitatory input to a target neuron


Removal of an inhibitory input to a target neuron

How do you permit desired movement and inhibit unwanted movements?

Activating direct or indirect pathway for gpi

DA effect on direct pathway

DA excites D1 striatal neuronsuppresses gpiless inhibition on thalamic neuronsactivate CST, not really any altered affect, just a bit more excitation

DA effect on indirect pathway

DA inhibits D2 striatal neuronremove inhibition from gpe to activateshutdown subthalamic neuronless excitatory on gpi/snrdecreased inhibitory output to thalamusincreased activity in CST, DA has excitatory effect on both direct/indirect pathway

brain anoxia

If you decrease activity in subthalamus then?

You have increased activity in CST

Parkinson’s disease

Gain of function changes in 2 genes (alpha-synuclein and parkin which aids in clearing damaged proteins), environmental toxins, loss of DA in snc, tremor at rest (4-5 sec), cogwheel rigidity (both flexor/extensor activated at same time), akinesia (impaired initiation of movement), bradykinesia (reduced amplitude/velocity of voluntary movement), effect is primarily on INDIRECT pathway (increased activity in subthalamus and decreased activity of CST)

Dopamine depletion

Rapid/profound loss of spines and glutamatergic synapses on medium spiny neurons expressing D2 receptors, D2 receptor signaling inhibits CA channels opening usually but without this ca enters loss of spines loss of glutamatergic synapses reduction in dendritic length/branching

brain anoxia

Treating parkinson’s disease

Ingestion of L-DOPA (systemic effects, while blocking rigidity may induce hyperkinesia), lesion subthalamus, DBS (to alter activity of neurons, gene therapy

Edit movement disorders- lynn 1 question


Tremor types

Resting (3-7 hz, parkinsons), postural/sustention (6-11 hz, essential or drug-induced), intention (3-7 hz, cerebellar disease, as they come near a target)


Slow writhing movements


Sudden brief irregular jerks associated with damage to striatum


Abrupt high amplitude violent choreic movements (subthalamic)


Co-contraction of agonist/antagonist m. Groups causing intermittent/persistent abnormal posture


Sudden twitch-like muscular contractions

brain anoxia


Arrhythmic lapse of sustained posture, see this in liver cirrhosis


Rapid brief stereotyped jerks most often in face and headn/neck, expecially in childhood

Parkinson’s disease

TRAP- tremor (pill rolling then supination/pronation, only 70% have this though), rigidity, akinesia/hypokinesia (slowness of voluntary movement and reduction of automatic movement), postural instability (shoulders not over base, asymmetric, gait abnormalities, festination, retropulsion)

Edit movement disorders- lynn 2 question


Lewy bodies

Eosinophilic intraneuronal inclusion bodies within CNS

PD pathology

Loss of pigmentation and dopaminergic neurons in SN (and GP/putamen etc), disturbance in balance between inhibitory DA and excitatory ach influence on GABA neuron in striatum

brain anoxia


Taken up by astrocytes and kicked back out to extracellular space and taken up by DA neurons to destroy mitochondriacell death

Essential tremor

Most common cause of tremor, age of onset is 5th decade on average, autosomal dominant familial, sporadic (benign essential tremor), senile tremor (65 years old), distual upper extremities primarily, wrist and fingers, elicited best with arms in sustention, no other TRAP features

Essential tremor tx.

Ethanol challenge, beta blockers, phenobarbital, amantadine, DBS

Tardive dyskinesia

Hyperkinetic movement, usually choreic, orofacial dyskinesia is most common (tongue protrusion/lip-smacking/chewing), etiology is DA receptor supersensitivity vs. DA overactivity due to hypocholinergic state

brain anoxia

Huntington disease

Loss of GABA neurons in striatum, AD on xsome 4, abnormal CAG repeat number, atrophy of head of caudate, onset is extremely variable, personality change/dementia/chorea/ataxia/ death

Wilson disease

Hepatolenticular degeneration, AR disorder of copper metabolism on xsome 13, gene ATP7B copper-binding atpase, defective binding of cu to transport protein, toxic deposition in brain (GP/putamen)/kidney/liver, presents in teens, sxs. Are hepatic dysfunction, renal acidosis, anemia and neurologic (wingbeating proximal tremor, facial grimace, dysarthria, ataxia, chorea)

Kayser fleischer rings

Corneal copper deposition seen with slit lamp in wilson’s disease

Dx./tx. Wilson’s disease

Serum copper/ceruloplasmin levels low, 24 hour urine cu excretion high, reduce dietary cu, chelation, zinc blocks dietary absorption, screen relatives

brain anoxia


Simple motor (eye blinks/rolling, shoulder shrugs, lower facial twitching), or simple vocal (grunts/squeaks etc), or complex vocal (phrases out of context, echolalia or repeating words), either primary disorder or secondary to trauma/drugs/encephalitis/toxins/wilson’s disease


Multiple motor and 1+ vocal tics at one time, may occur many times per day for 1 year, changes over time, onset before 21, abnormal circuitry and unwanted movements are not suppressed, associated with genetics or psych conditions, treat with DA receptor antagonist