BASAL NUCLEI (BASAL GANGLIA) CLAUSTRUM 2. Outflow from basal n.

CLAUSTRUM 2. Outflow from basal n. is channeled through globus - SN neuron degeneration → ↓ release of dopamine w/in
- Masses of GM w/in each cerebral hemisphere - Thin sheet of GM separated from lateral surface of pallidus → influences activities of motor areas of corpus striatum → hypersensitivity of dopamine
- Control of posture and voluntary movement lentiform n. by EC; unknown function cerebral cortex or other motor centers in brainstem receptors in postsynaptic neurons in the stratum
- No direct input/output connections to SC - Laterally: subcortical WM of insula - Basal n. influence cerebral cortex to control movements; - Characteristic S&S:
no direct control through descending pathways to the 1. Tremor: due to alternating contraction of agonists
Neurologic structure Basal nucleus CONNECTIONS OF CORPUS STRIATUM AND GLOBUS brainstem and spinal cord and antagonists; slow and most obvious when limbs
Caudate nucleus Caudate nucleus PALLIDUS o Assist in regulation of voluntary movement and are at rest and disappears during sleep
Lentiform nucleus Globus pallidus + putamen - Caudate n. and putamen: main sites for receiving input learning of motor skills ▪ NB: diff. w/ cerebellar disease (intention tremor
Claustrum Claustrum to the basal nuclei ▪ Primary motor cortex damage: cannot perform → purposeful active movement attempted)
Corpus striatum Caudate n. + lentiform n. - Globus pallidus: major site from which the output leaves fine discrete movements of contralateral limbs 2. Rigidity: present to equal extent in opposing muscle
Neostriatum (striatum) Caudate n. + putamen the basal nuclei ▪ Crude movement of contralateral limb possible groups (unlike rigidity from UMN lesions)
Amygdaloid body Amygdaloid n. - Receives no direct input from or output from SC ▪ Corpus striatum damage: paralysis of remaining ▪ Plastic rigidity – tremor is absent
movements of the contralateral side of body ▪ Cogwheel rigidity – tremor is present; jerky
Corpus Striatum Afferent Fibers o Assist by preparing the movement of the body 3. Bradykinesis: difficulty initiating (akinesia) and
CORPUS STRIATUM
- Corticostriate fibers: all parts of cerebral cortex send ▪ By controlling axial and girdle movements of the performing new movements
- Lateral to thalamus; divided by internal capsule →
axons to caudate n. and putamen body and positioning of proximal part of limbs ▪ Slow movement, face no expression, slurred and
caudate and lentiform nucleus
o Each part of cerebral cortex projects to a specific part ▪ ↑ activity in globus pallidus before active unmodulated voice; arm swinging lost on walking
- GM passing through IC and connecting the caudate
of caudate-putamen complex movement take place in the distal limb muscle 4. Postural disturbances
nucleus and putamen of lentiform nucleus → striated
o Most projections are from cortex of the same side ▪ Preparatory function enables trunk and limbs to ▪ Standing with a stoop; arms are flexed
Caudate Nucleus
o Largest input: sensory motor cortex be appropriately placed before primary motor ▪ Walk short steps and often unable to stop → may
- Large C-shaped mass of GM close to the lateral ventricle;
o Neurotransmitter: glutamate part of cerebral cortex activates discrete break into a shuffling run to maintain balance
lies lateral to thalamus
- Thalamostriate fibers: intralaminar nuclei of thalamus movements in the hands and feet 5. No loss of muscle power nor sensibility occurs
- Lateral surface related to lentiform n.
send many axons to the caudate n. and putamen ▪ Corticospinal tracts normal →
- Divided into:
- Nigrostriatal fibers: axons from SN sent to caudate n. and CLINICAL NOTES • (+) abdominal reflex
o Head: large and rounded; forms the lateral wall of
ant. horn of lateral ventricle
putamen; liberate dopamine at their terminals - Basal n. disorders: • (-) Babinski reflex
▪ Continuous inf. w/ putamen of lentiform n.
o Neurotransmitter: dopamine o Hyperkinetic: excessive and abnormal movements • Normal DTR
o Inhibitory fibers ▪ Chorea, athetosis, ballism - Known causes of PD:
▪ Corpus striatum: superior to union of caudate n.
- Brainstem striatal fibers: fibers from BS end in caudate n. o Hypokinetic: lack or slowness of movement o Postencephalitic parkinsonism: viral encephalitis →
and putamen; striated due to strands of GM in IC
and putamen; liberate serotonin at their terminals Chorea: involuntary, quick, jerky, irregular movements that basal n. damage
o Body: long and narrow and continuous w/ head in
o Neurotransmitter: serotonin are nonrepetitive; e.g., swift grimaces/sudden movement o Iatrogenic parkinsonism: antipsychotic drugs (e.g.,
the region of the interventricular foramen
o Inhibitory fibers of head or limbs phenothiazines); meperidine analogues; CO and Mg
▪ Forms part of the floor of body of lateral ventricle
- Huntington Disease: AD disease w/ onset in adult life poisoning
o Tail: long and slender and continuous w/ body in the
Corpus Striatum Efferent Fibers o Death occurs 15 to 20 years after onset o PD treatment: ↑ brain dopamine level
region of the post. end of thalamus
- Striatopallidal fibers: from caudate n. and putamen to o Gene defect on chromosome 4 → huntingtin ▪ L-Dopa: precursor; taken up by dopaminergic
▪ Follows contour of lateral ventricle
globus pallidus o Affects men and women equally neurons in basal n. and converted to dopamine
▪ Continues forward in the roof of the inferior horn
o Neurotransmitter: GABA o Characteristic S&S: ▪ Selegiline: ↓MAO-B → ↓dopamine breakdown;
of lateral ventricle
- Striatonigral fibers: from caudate n. and putamen to SN ▪ Choreiform movements slows SN dopa-secreting neuron degeneration
▪ Terminates ant. in the amygdaloid nucleus
o Neurotransmitter: GABA/Ach/substance P ▪ Progressive dementia ▪ Pallidotomy: surgical lesions in globus pallidus
Lentiform Nucleus
o GABA-, substance P-, and ACh-secreting neurons of can alleviate parkinsonian signs; used if no longer
- Wedge-shaped: base → lateral; blade → medial
Globus Pallidus Afferent Fibers striatonigral inhibiting pathway degenerate → responsive to medical treatment
- Divided by a vertical plate of WM into
- Striatopallidal fibers: from caudate n. and putamen to ▪ Dopa-secreting neuron of SN become overactive Drug-Induced Parkinsonism
o Putamen (darker, larger, lateral); continuous w/ head
globus pallidus ▪ Nigrostriatal PW inhibit caudate n. and putamen - Disappears once agent is withdrawn
of caudate n. inf. at its ant. end
o Neurotransmitter: GABA ▪ Inhibition → abnormal movements - Phenothiazines and butyrophenones: blocks striatal
o Globus pallidus (lighter, smaller, inner); due to high
o CT: enlarged lateral ventricles due to caudate n. dopamine receptors (D2); given for psychotic behaviors
conc. of myelinated nerve fibers
Globus Pallidus Efferent Fibers degeneration - Tetrabenazines: deplete striatal dopamine
- Deep in WM of cerebral hemisphere and related
- Pallidofugal fibers: - Sydenham Chorea (St. Vitus dance): disease of childhood
medially to IC (IC separates caudate n. to thalamus)
o Ansa lenticularis → pass to thalamic n. o Rapid, irregular, involuntary movements of limbs, Athetosis: slow, sinuous, writhing movements that most
- Lateral to external capsule (sheet of WM; separates
o Fasciculus lenticularis → pass to subthalamus face, and trunk; associated w/ rheumatic fever commonly involve distal segments of the limbs
lentiform n. to claustrum)
o Palidotegmental fibers → end in caudal tegmentum ▪ Antigen of strep similar to proteins in striatal - Degeneration of globus pallidus occurs w/ breakdown of
- Claustrum separates EC from insula
o Pallidosubthalamic fibers → pass to subthalamic n. neuron membrane → AB attacks membranes circuitry involving basal n. and cerebral cortex
▪ Results in choreiform movements (transient)
AMYGDALOID NUCLEUS
BASAL NUCLEI FUNCTIONS Hemiballismus: involuntary movement on one side of body
- In the temporal lobe close to uncus; part of limbic system
- Corpus striatum receives afferent information from: - Usually involve proximal limb musculature → flies out of
- Influence body’s response to environmental changes
o Most of cerebral cortex, thalamus, subthalamus, control in all direction
through its connections (fear → ∆ HR, BP, skin color, RR)
brainstem, substantia nigra - Lesion: usually a small stroke in the opposite subthalamic
o Info integrated w/in corpus striatum then output nucleus or its connections
SUBSTANTIA NIGRA AND SUBTHALAMIC NUCLEI
passes back to the same areas Parkinson Disease: progressive disease of unknown cause
- Substantia nigra: dopaminergic and inhibitory; many
- Circular pathway: - Age of onset: bet. 45 and 55 years
connections to corpus striatum
1. Information from premotor and supplemental areas - Neuronal degeneration in SN and to a lesser extent –
- Subthalamic nuclei: glutaminergic and excitatory; many
of motor cortex, primary sensory cortex, thalamus, globus pallidus, putamen, and caudate n.
connections to globus pallidus and substantia nigra
and brainstem → initiation of basal n. activity