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NE > Basal Ganglia (Stephens) > Flashcards

Basal Ganglia (Stephens) Flashcards

1
Q
  • involved in crude, stereotyped associative movements of the axial and proximal limb musculature
  • initiates movement through subcortical loops, providing framework for all focal motor activity
  • also plays role in facilitation of motor centers and activation of reflex arcs
  • primary influence of this system is on primary and premotor cortices
  • principal subcortical loop is striatal loop and one of the indirect descending pathways, the corticorubrospinal pathway
A

extrapyramidal system (EPS)

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2
Q

What are the components of the basal ganglia?

A
  • caudate nucleus
  • putamen
  • striatum: caudate nucleus + putmen
  • globus pallidus: internus and externus
  • lentiform nucleus: globus pallidus + putamen
  • thalamus: ventral anterior nucleus and ventral posterior nucleus
  • subthalamic nucleus
  • substantia nigra: zona compacta and zona reticularis
  • red nucleus (of the RF)
  • nucleus accumbens
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3
Q
  • located on the lateral aspect of the genu of IC
  • along w/ the substantia nigra, this is the principal source of efferents from basal ganglia
  • part of the diencephalon
A

globus pallidus

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4
Q
  • elongated tear drop shaped nucleus located on surface of inner curvature of lateral ventricle
  • separated from putamen by IC but functionally similar
A

caudate nucleus

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5
Q
  • largest nucleus of the BG, located lateral to globus pallidus beneath anterior limb of IC
  • derived from telencephalon and, along w/ the caudate nucleus, forms the striatum
A

putamen

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6
Q
  • two parts: zona compacta and zona reticularis
  • reticularis: anterior portion, contains serotonin and GABA NT’s, neurons do not contain melanin, source of most of efferents of this structure
  • compacta: contains dopamine and melanin NT’s, these neurons are principally destroyed in Parkinson’s dz
A

substantia nigra

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7
Q
  • subdivision of the RF, located in the center of midbrain tegmentum
  • surrounded by fibers from superior cerebellar peduncle
  • most of these fibers project to inferior olivary nucleus (ION) via central tegmental fasciculus as part of the subcortical loop to the cerebellum
  • part of the projection pathway from dentate nucleus to the ventral anterior thalamic nucleus
A

red nucleus

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8
Q
  • involved in the movements of proximal musculature, may be more significant during crawling phase of human infants
  • this tract descends to cervical SC
  • function is redimentary in humans but may play a role in neurorehab after CST injury
A

rubrospinal tract

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9
Q

What signs and symptoms would present in an individual w/ unilateral lesion of the red nucleus and midbrain tegmentum?

A

(Benedikt’s syndrome)

  • ipsilateral oculomotor palsy
  • contralateral motor dysfunction: tremor, ataxia, or choreiform movements

(contralat sx due to involvement of crossed fibers of superior cerebellar peduncle that course through red nucleus)

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10
Q
  • structure mainly formed by rostral extension of the midbrain RF
  • reciprocally connected to globus pallidus
  • regulates output of BG
A

subthalamus

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11
Q

What signs/symptoms would a unilateral lesion of the subthalamus result in?

A

contralateral hemiballism of upper and lower extremity

(violent involuntary limb movements, on one side of the body, can cause significant disability; always a/w hypotonus)

(may be caused by reduction/loss of inhibition (GABA) on globus pallidus by subthalamus)

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12
Q
  • small accumulation of gray matter between putamen and caudate, below anterior limb of IC
  • this structure + the olfactory tubercle = ventral striatum
  • links amygdala and hippo to dorsomedial nucleus of thalamus and globus pallidus
  • may play a role in motivational and emotional aspects of movement
  • dopaminergic neurons of mesolimbic pw project into GABAergic neurons of this structure
  • this structure is involved w/ encoding of new motor programs, and cognitive processing of aversion, motivation, reward, and reinforcement learning
  • plays a significant role in addictive behavior
A

nucleus accumbens

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13
Q

What are the 2 divisions of the pallido-thalamic fibers?

A

dorsal and ventral divisions of the ansa lenticularis

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14
Q
  • commonly called the lenticular fasciculus (H2)
  • these pallido-thalamic fibers join w/ the ventral division and form the thalamic fasciculus
  • these fibers are also shared w/ the dentato-thalamic and dentato-rubro-thalamic pathways
  • some of these fibers also project to cerebellum
A

dorsal vision of the ansa lenticularis

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15
Q
  • usually referred to as the ansa lenticularis
  • most of these fibers are pallido-thalamic fibers, which join w/ the lenticular fasciculus to form the thalamic fasciculus
A

ventral divison of the ansa lenticularis

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16
Q

The EPS does not project fibers below the level of the ______; most fibers are directed toward the _______.

A

The EPS does not project fibers below the level of the midbrain; most fibers are directed toward the cortex.

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17
Q
  • non dopaminergic fibers that originate in the zona reticularis of the SN and term in the VA and VL thalamic nuclei
A

nigro thalamic fibers

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18
Q

What is the importance of distinguishing between where the globus pallidus and substantia nigra fibers term in the VA and VL nuclei?

A
  • they do not term in the same area of VA and VL
  • important distinction in stereotaxic surgery for Parkinson’s dz
19
Q
  • dopaminergic fibers that originate in zona compacta of the SN and term in the striatum
  • neurons in this area of the SN are destroyed in Parkinson’s dz
  • in comparison, destruction of the inhibitory, GABA-nergic fibers in the striatonigral fibers are involved in Huntington’s chorea
A

nigrostrial fibers

20
Q

Describe the pallidal and substantia nigra loops:

A
  • play important roles in initiating motor movement patterns and integrating them w/ cerebellum, cerebral cortex, and limbic system
  • cortico-striatal fibers are excitatory, pallido-thalamic and nigrothalamic fibers are inhibitory on motor nuclei of thalamus
21
Q

Describe the cerebellar loop:

A

cerebellum adjusts intensity of motor movement pattern to appropriate level of task

22
Q

Summary of the cerebellar and striatal loops:

A
23
Q

Integration of the motor and limbic systems:

A
24
Q
  • involves the motor neurons of the anterior horns and the cranial nerve motor nuclei
  • sx: pyrexia, headache, vomiting, neck stiffness, and pain in back/limbs
  • patient can fully recover, although it may result in long term paresis/paralysis
  • severe inflammation, vasodilation, edema, and macrophagic activity (causing neuron death and astrocytic gliosis)
A
25
Q

What are symptoms and possible causes of LMN paralysis?

A
  • symptoms: flaccid paralysis (atonia and areflexia), fasciculations, atrophy
  • possible causes: poliomyelitis, ALS
26
Q

What are some symptoms and possible causes of UMN paralysis?

A
  • symptoms: spastic paralysis (hypertonia, hyperreflexia), Babinski sign, clonus
  • possible causes: spinal cord transection, ALS
27
Q
  • sometimes referred to as UMN paralysis
  • characterized by hypertonia, hyperreflexia, Babinski sign, clonus, and disuse atrophy
  • most pronounced in distal limb musculature in the upper extremities
A

spastic paralysis

28
Q
  • etiology of condition unknown, thought to be caused by defect in glutamate metabolism
  • a/w damage of UMN (anterior horn cells, hypoglossal nucleus, nucleus ambiguus, facial motor nucleus) and/or LMN (chronic progressive degeneration of corticospinal tracts)
  • leads to paresis and atrophy of the intrinsic muscles of hands followed later by arms and shoulder musculature
  • patients may develop dysarthria, dysphagia, and paresis of tongue
  • involvement of CST leads to spastic paralysis, hyperreflexia, and Babinski sign
  • no sensory deficits seen due to disease itself
  • death due to bulbar paralysis (i.e. vital respiratory centers)
A

amyotrophic lateral sclerosis (ALS)

29
Q
  • subcortical degeneration involving substantia nigra, globus pallidus, upper brainstem nuclei (mainly RF) and occasionally the postganglionic sympathetic neurons
  • sx can be caused by multiple things, most common are: postencephalitic, arteriosclerotic, and drug-induced
  • tardive dyskinesia (repetitive involuntary licking and smacking movements of lips): caused by over-titration of long-term neuroleptic meds; may result from neuroleptic-induced dopamine supersensitivity in nigrostriatal pw w/ the D2 dopamine receptor being most affected
  • other signs/symptoms: bradykinesia, tremor during rest, rigidity, masked face, postural embarrassment
A

Parkinson’s disease

30
Q
  • paucity of movement w/ difficult initiating movement
  • varying degrees of difficulty initiating motor movement patterns, especially gait patterns
  • very restrictive to patient
  • often seen in Parkinson’s patients
A

bradykinesia

31
Q
  • tremor that is present during rest, usually present in distal upper extremity and possibly lower jaw
  • slow tremor that is absent or reduced during movement and aggravated by emotions
  • often seen in Parkinson’s patients
A

pill rolling tremor

32
Q
  • abnormal passive resistance to movement in all directions
  • most disabling sx in Parkinson’s patients
A

rigidity

33
Q
  • mimetic expressions and a positive glabellar reflex (tapping on patient’s forehead w/ finger results in no attenuation of blinking w/ repetition)
  • often seen in Parkinson’s patients
A

masked face

34
Q
  • initially, Parkinson’s patients respond to backwards threat to standing posture w/ short, choppy multiple steps
  • later, feet will remain fixed to the floor
A

postural embarrassment

35
Q
  • autosomal dominant motor disorder, localized to mutation on short arm of chromosome 4
  • principal areas of degeneration are corpus striatum and cerebral cortex
  • sx may be due to excessive dopaminergic influence in degenerated striatum or loss of inhibition from GABAnergic neurons of striatonigral pathway
  • common symptoms: dementia, chorea, and behavioral disturbances (depression, irritability)
  • choreiform movements: sudden, irregular, involuntary, jerky, purposeless movements
A

Huntington’s chorea

36
Q

Parkinson’s disease

  • signs/sx:
  • due to:
A

Parkinson’s disease

  • signs/sx: bradykinesia, tremor during rest, rigidity, masked face, glabellar reflex, postural embarrassment, autonomic effects, cognitive changes
  • due to: degeneration of substantia nigra, globus pallidus, brainstem RF, and postganglionic sympathetic neurons
37
Q

Huntington’s chorea

  • signs/sx:
  • due to:
A

Huntington’s chorea

  • signs/sx: onset 30-40, choreiform movements, severe dementia, choreoathetosis, behavioral disturbances
  • due to: autosomal dominant mutation on chromosome 4; degeneration of corpus striatum and cerebral cortex results in excessive dopaminergic influence in the degenerated striatum or loss of inhibition from the GABAnergic neurons of the striatonigral pw
38
Q

Hemichorea

  • sx:
  • due to:
A

Hemichorea

  • sx: unilateral choreiform movements
  • due to: vascular lesion in the basal ganglia
39
Q

Athetosis

  • sx:
  • due to:
A

Athetosis

  • sx: slow, involuntary, writhing movements of limbs/face
  • due to: degeneration of striatum
40
Q

Hemiballism

  • signs/sx:
  • due to:
A

Hemiballism

  • signs/sx: conralateral violent, flailing, movements of the proximal musculature of both upper/lower extremities
  • due to: unilateral lesions of subthalamus result in reduction/loss of glutamate inhibition upon globus pallidus
41
Q
  • caused by lesion in Broca’s speech area in dominant hemisphere
  • language disturbance in which there are errors in grammar and word choice
  • patient unable to speek fluently b/c they cannot select appropriate grammar and/or words
A

Broca’s aphasia (expressive or nonfluent motor aphasia)

42
Q

Spastic hemiplegia indicates involvement of which of the following?

A. Corticospinal tract

B. Lateral reticulospinal tract

C. Spinal lemniscus

D. Genu of internal capsule

E. Ventral roots

A

A. Corticospinal tract

B. Lateral reticulospinal tract

C. Spinal lemniscus (lesion=contralateral loss of pain/temp in body)

D. Genu of internal capsule (these are corticobulbar fibers: lesion= contralateral supranuclear facial palsy)

E. Ventral roots

(CST are UMN, lesion here results in contralateral spastic hemiplegia: hyperreflexia, hypertonia, paralysis, and disuse atrophy)

(lesions of ventral roots cause LMN paralysis of associated motor dermatome: atonia, areflexia, fasciculation, and flaccid paralysis)

43
Q

Supranuclear facial palsy indicates involvement of which of the following?

A. Facial nerve

B. Corticobulbar tract

C. Corticospinal tract

D. Posterior limb of internal capsule

E. Rubrospinal tract

A

Supranuclear facial palsy indicates involvement of which of the following?

A. Facial nerve

B. Corticobulbar tract

C. Corticospinal tract

D. Posterior limb of internal capsule

E. Rubrospinal tract

(corticobulbar fibers originate in head region of precentral gyrus, course through genu of IC and cerebral peduncles as uncrossed CBT (unilat lesions result in contralateral supranuclear facial palsy), decussate in lower pons between V and VI and descend in lower brainstem as crossed CBT (unilat lesions below decussation may result in ipsilat cranial nerve palsies))

44
Q

Bilateral atonia, areflexia and flaccid paralysis involving the C7-T1 motor dermatomes indicates involvement of which of the following?

A. Anterior horn neurons

B. Anterior white commissure

C. Dorsal roots

D. Lateral Corticospinal tract

E. Posterior limb of internal capsule

A

Bilateral atonia, areflexia and flaccid paralysis involving the C7-T1 motor dermatomes indicates involvement of which of the following?

A. Anterior horn neurons

B. Anterior white commissure

C. Dorsal roots

D. Lateral Corticospinal tract

E. Posterior limb of internal capsule

(these findings are characteristic of LMN paralysis)

NE (36 decks)

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