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3RD SHIFT_NL  Caudate nucleus  head, body, tail

BASAL GANGLIA Internal capsule  separates lentiform


- Regulation of movement from caudate nucleus
- Connectivity w/ cerebrum,
thalamus, spinal cord, brainstem 2. Caudate nucleus
- No direct connections w/ spinal cord  green color
- Collection of subcortical gray matter  large c-shaped
(situated within each hemisphere)  will end in amygdaloid body
 head, body, tail
 corpus striatum
 amygdaloid nucleus (anatomical)  head of caudate
 claustrum (anatomical) - Lateral wall of anterior horn of
lateral ventricle
closely related but should not be included: - continuous inferiorly with putamen
(functional) of lentiform nucleus (striatum)
 subthalamic nuclei - superior to that union (strands of
 substantia nigra gray matter pass through internal
 red nucleus capsule = striated appearance
(corpus striatum) / union
Gray matter  outermost layer/cortex
White matter  subcortical area  body of caudate nucleus
Basal ganglia  subcortical gray matter - long and narrow
- continuous with head sa
ORGANIZATION interventricular foramen
Striatum  caudate nucleus and putamen - floor of the body of lateral ventricle
Lentiform nucleus  Globus pallidus +
putamen  tail of caudate nucleus
Amygdaloid nucleus  integral part of - long and slender
limbic system - continuous with body sa posterior
end of thalamus
1. CORPUS STRIATUM - terminates anteriorly in the
- Caudate nucleus + lentiform nucleus amygdaloid nucleus
(putamen + globus pallidus)
- Lateral to thalamus LENTIFORM NUCLEUS
- May mga pumapasok na fibers - wedge shaped
(internal capsule)  globus pallidus (lighter) – white
- Almost completely divided by matter ; myelinated
internal capsule  putamen – continuous with head of
- Strands of gray matter caudate nucleus ; larger
- Where info is integrated
Putamen  outer part of lentiform (lateral)
 Lentiform  most lateral (GP + External capsule  White matter outside
putamen) lentiform nucleus
Claustrum  gray matter lateral to external CONNECTIONS OF STRIATUM AND GLOBUS
capsule PALLIDUS
- separates external capsule from
subcortical white matter of insula Neostriatum
(extreme capsule)  caudate nucleus + putamen = afferent
- unknown function (receiving input)

Internal capsule  medial to lentiform  globus pallidus (medial) = efferent


nucleus (output leaves basal nuclei)

Extreme capsule  lateral to claustrum AFFERENT FIBERS

AMYGDALOID NUCLEUS 1. Corticostriate fibers (glutamate)


- temporal lobe; close to uncus  all parts of cerebral cortex send axons
- limbic system  papasok sa basal ganglia
- body’s response to environmental  papasok sa caudate nucleus + putamen
changes  each part of cerebral cortex projects to
- heart rate, blood pressure, skin specific part of caudate-putamen complex
color, rate of respiration (ipsilateral)
 largest input is from sensory-motor
Substantia nigra (midbrain) & subthalamic  excitatory
nuclei (diencephalon)
 not anatomically related but functionally 2. Thalamostriate fibers
related to basal nuclei - Intralaminar nuclei of thalamus 
caudate-putamen
 substantia nigra
- neurons are dopaminergic and 3. Nigrostriatal fibers (dopamine)
inhibitory - From midbrain
- many connections to corpus - Substantia nigra  caudate-
striatum putamen
- Liberate dopamine at terminals
 Subthalamic nuclei - Inhibitory
- very small; cannot be seen by naked -  pag nasira/kulang dopamine =
eye excessive movements
- glutaminergic and excitatory -  parkinsons disease
- connections to globus pallidus and
substantia nigra 4. Brainstem striatal (serotonin)
- Ascending fibers from brainstem 
If may lesions/injury/connection  caudate-putamen
movement problems - Liberate serotonin
- Inhibitory
 Pallidosubthalamic (pass to
CORPUS STRIATUM EFFERENT FIBERS subthalamic nuclei)
 MAY PABALIK KUNG SAAN SILA GALING;
RECIPROCAL FUNCTIONS OF BASAL GANGLIA
 info received from premotor,
GLOBUS PALLIDUS  only part ng corpus supplemental areas of motor cortex,
striatum that gives efferent primary sensory cortex, thalamus,
 triangle brainstem
 GABA is inhibitory  posture and movement
 amygdaloid and claustrum di kasama
1. Striatopallidal fibers (GABA) functionally
- Caudate-putamen to globus pallidus  control muscular movements by
- Y-aminobutyric acid (gaba) influencing cerebral cortex
- Inhibitory  contralateral weakness (pag may
problem sa basal ganglia)
2. Striatonigral fibers  driver para I command ang cerebral
(GABA/ACh/SUBSTANCE P) cortex based sa natanggap na stimulus
- pass directly from caudate-putamen (initiate)
to substantia nigra  activated for precise movements
- di dinadaanan ang globus pallidus
- GABA or Ach, substance P CLINICAL NOTES
- should work in unison para exact
yung normal movement HYPERKINETIC  excessive and abnormal
movements (chorea, athetosis, ballism)
AFFERENT FIBERS FOR GLOBUS PALLIDUS
HYPOKINETIC  lack, slowness of
 Striatopallidal fibers (GABA) movement
- Caudate nucleus-putamen to globus
pallidus  Parkinsons  both hypo and
hyperkinetic
EFFERENT FIBERS FOR GLOBUS PALLIDUS (hypo) Diffucty in moving, standing up
(hyper) tremor
 Pallidofugal fibers
- Complicated Chorea  biglang mag jjerk (magssnap neck
- Divided into groups sa isang side, pipitik kamay, or tataas
- 2 connections go to subthalamus shoulder)
- From globus pallidus  involuntary, quick, jerky, irregular,
nonrepetitive
 Ansa lenticularis (pass to thalamic
nuclei) Huntington disease  genetic ; adult life
 Fasciculus lenticularis (pass to  affects men and women after children
subthalamus)  death occurs after 15 to 20 years
 Pallidotegmental (terminate in  defect on chromosome 4  encodes
caudal tegmentum of midbrain) huntingtin (protein)
 the codon (CAG encodes glutamine) is  reduction of release of dopamine
repeated many times (inhibitory)  hypersensitivity of dopamine
 degeneration of inhibitory (GABA, receptors in post synaptic neurons in corpus
SUBSTANCE P, Ach) sa strionigral striatum
 from striatum to midbrain (substantia  nawawala yung dark pigmented neurons
nigra)  left is normal ; right is ABN substantia
 overactive dopamine nigra
 nigrostriatal pathway inhibits caudate-  needs PT and OT
putamen  tremor of one hand is initial
 when inhibition happens in caudate-
putamen = abnormal movements (chorea) SIGNS AND SYMPTOMS:
 Tremor
 Choreiform movements - Alternating contraction of agonist
 Progressive dementia and antagonist
- Slow ; resting tremors
Sydenham chorea (St. Vitus’ dance) - Disappears during sleep
 rapid, regular, involuntary (childhood)
 nagkakaroon ng competitive inhibition  Rigidity
 host’s antibodies combine and attack - Resistance to passive moments
system (rheumatic fever) ; streptococcal
bacteria  Bradykinesis
 happens to kids - Initiating (akinesia) and performing
 akala ng magulang they’re just dancing new movements is difficult
 serpentine movements - Slow movement, expressionless
 choreiform movements are transient = face, sluured and unmodulated
full recovery voice, no swinging or arms in
walking
Hemiballismus  Postural disturbances
- Involuntary movement confined to - Stoop, arms flexed
one side of the body - Short steps + unable to stop
- Proximal extremity ; limb flies out of - Shuffling run to maintain balance
control in all directions - No loss of power and sensibility
- Stroke occurs in opposite
subthalamic nucleus or connections Usually stage 3 – PT d/t fractures
(where smooth movements of body
are integrated)

Parkinson disease
 growing problem (BETWEEN 45 AND 55)
 neuronal degeneration in substantia
nigra, globus pallidus, putamen, caudate
nucleus
 dopamine will degenerate in midbrain
(substantia nigra)

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