Basal Ganglia

Front 1

what are the five basal ganglia and there subsequent subdivisions?

Back 1

caudate nu, putamen, globus pallidus, amygdala, and claustrum. The lentiform nu consists of the globus pallidus and putamen, the striatum contains the caudate nu and putamen, and the corpus striatum includes the caudate, putamen, and globus pallidus

Front 2

what is the blood supply of the corpus striatum? subthalamus? substantia nigra?

Back 2

medial and lateral striate, posteromedial, posteromedial and posterolateral and ant choroidal

Front 3

what is the tract for the basal ganglia motor system?

Back 3

substantia nigra to the striatum to the globus pallidus to the dorsal thalamus to the motor and premotor cortex

Front 4

what is the tract for the limbic system of the basal ganglia?

Back 4

ventral tegmental area to the ventral striatum (nu accumbens) to the dorsal thalamus to the frontal and limbic cortex.

Front 5

what will cause parkinsons? schizophrenia?

Back 5

decreased nigrostriatal dopamine (from substantia nigra to the striatum), increased mesolimbic dopamine (from ventral tegmental area of midbrain to the ventral striatum) OR decreased mesocortical dopamine (from midbrain ventral tegmental area to the frontal or limbic cortex)

Front 6

what are the functions of the motor system of the basal ganglia? the limbic system?

Back 6

planning, initation, facilitation, and suppression of movement. Mood, motivation and behavior

Front 7

in the motor part of the basal ganglia, what areas influence the striatum? the globus pallidus?

Back 7

all areas of the cerebral cortex connect to the striatum while the subthalamus also has input from the globus pallidus

Front 8

what nuclei in the dorsal thalamus does the motor system of the basal ganglia synapse?

Back 8

VL and VA

Front 9

what are all the connections in the motor system of the basal ganglia?

Back 9

corticostriatal, striatopallidal, pallidosubthalamic, subthalamopallidal, pallidothalamic, thalamocortical, nigrostriatal, raphestriatal, striatonigral, nigrothalamic, and thalamostriatal.

Front 10

glutamate is the NT used for what connections in the motor system of basal ganglia?

Back 10

thalamocortical, corticostriatal, and subthalamopallidal

Front 11

GABA is the NT used for what connections in the motor system of basal ganglia?

Back 11

striatopallidal and pallidothalamic

Front 12

dopamine is the NT used for what connections in the motor system of basal ganglia?

Back 12

nigrostriatal (note there are two synapse types, an inhibitory and an excitatory receptor type)

Front 13

serotonin is the NT used for what connections in the motor system of basal ganglia?

Back 13

the raphestriatal

Front 14

Ach is the NT used for what connections in the motor system of basal ganglia?

Back 14

the striatal interneuron between the corticostriatal and the striatopallidal

Front 15

suppression of movement in the basal ganglia movement system is mediated via what areas? faciliatation of movement?

Back 15

striatum and subthalamus. striatum and the substantia nigra

Front 16

function of the input to the striatum from the cortex?

Back 16

planning and initation of movement via glutamate

Front 17

the striatal interneuron function is?

Back 17

sporadically active and uses Ach to modulate and suppress DA activity

Front 18

describe the function of DA and the striatal output.

Back 18

DA from the substantia nigra will always facilitate movement via striatal output, but it uses two different DA receptors and thus 2 pathways. The indirect pathway has inhibitory DA receptors that inhibit the GABAergic striatopallidic neurons thus allowing the GABAergic pallidosubthalamic neurons to fire and thus inhibit the glutamatergic subthalamopalladic neurons preventing the GABAergic pallidothalamics from firing thus allowing movement (without DA these neurons are excited to fire thus inhibiting movement). The direct pathway has excitatory DA receptors that stimulates
GABAergic striatopallidic neurons that inhibit the GABAergic pallidothalamic thus allowing movement.

Front 19

the output of the thalmocortical fibers is to do what?

Back 19

allow movement via glutamate.

Front 20

what is dyskinesia? hypokinesia? akinesia? bradykinesia? hyperkinesia?

Back 20

involuntary movement disorders. decrease in movement and increase in tone. absence of movement (impaired initiation or cesation of movements). Reduced velocity and amplitude of movement. increased movement and decreased tone.

Front 21

all unilateral basal ganglia have symptoms on what side of the body?

Back 21

the contralateral side.

Front 22

hypokinesia occurs when what NT's are imbalanced? hyperkinesia?

Back 22

DA < GABA + Ach.
DA > GABA + Ach

Front 23

what is an athetoid movement? choreiform? ballistic? dystonia? akathisia? myoclonus?

Back 23

slow, twisting movements of distal muscles. brisk, fast and dancelike movements. flailing and fast crazy movements. sustained or repetive muscular contraction or cramping often resulting in joint distortions. movement acted out by an inner feeling for the need to move (often induced by antipsychotic medications). lightning like intermittent muscle jerks of unknown origin.

Front 24

what two involuntary movements from the basal ganglia disorders can be suppressed.

Back 24

tic and akathisia

Front 25

what are the symptoms of parkinsons?

Back 25

akinesia, bradykinesia, festination (accleration of gait), resting tremor, rigidity (both plastic and cogwheel), impaired postural (vestibular) reflexes as well as cognitive and emotionl disorders.

Front 26

the lesion location for parkinsons is where? what is reduced?

Back 26

substantia nigra and loss of dopaminergic cells

Front 27

what are the etiologies of parkinsons?

Back 27

idiopathic (genetic) plus environmental factors. Secondary etiology maybe from certain chemicals like CO, cyanide, tetrohydropyridines. Trauma and stroke have also been shown to cause parkinson symptoms

Front 28

what are the five stages of parkinsons?

Back 28

unilateral, bilateral with shuffling gate, postural reflex impaired, postural reflexes are poor (falls down), chair or bedridden

Front 29

the classic reaction to L dopa treatment for parkinsons is what?

Back 29

the on-off reaction; movement is in spurts of on when dopamine is high then to off when it is low.

Front 30

what are the sign and symptoms of huntington's chorea?

Back 30

choreoform and/or choreoathetoid movements throughout the body, hyperkinesia, hypotonia, dementia

Front 31

what is the etiology of huntington's chorea?

Back 31

AD mutation

Front 32

what is the major target of huntington's?

Back 32

the indirect pathway thus less GABA and more DA ratio

Front 33

what are the signs and symptoms of hemiballismus?

Back 33

ballistic movements in proximal musculature in one or both contralateral extremities, a hyperkinesia

Front 34

what is the etiology of hemiballismus?

Back 34

occlusion of posteromedial central artery resulting in a lesion of the subthalamus. Thus less GABA and more DA ratio

Front 35

what is the lesion location of dystonic contractures?

Back 35

it varies, but it is usually seen in late stages of some basal ganglia disorders like parkinsons and cerebral palsy.

Front 36

what are characteristcs of tardive dyskinesia?

Back 36

seen in some schizophrenic patients treated with antipsychotics (increase sensitivity to DA). Choreoathetoid movements simillar to Huntingtons.

Front 37

what are the characteristics of cerebral palsy?

Back 37

due to hypoxic or ischemic events inutero resulting in a variety of motor system impairments.

Front 38

what are the characteristics of Gilles La Tourette syndrome?

Back 38

usually affects young males and characterized by multiple tics and rarely involuntary vocalization of emotionally sparked remarks (corporalea). shows the close association between the limbic and motor systems. Usually have ADHD and OCD.

Front 39

Characteristics of OCD?

Back 39

cannot supppress the repeated execution of a motor task. May have to do with serotonin bc SSRI's help out. Along with tics and sydenham's chorea, has been associated with strepptococcus A infections and thus maybe the result of an autoimmune cross-reaction process.