Imbalance of movement facilitation and inhibition What are the three ways output nuclei decrease movement? The most prevalent inhibitory neurotransmitter in the CNS is: Tone is generally ______________ with hyperkinesia What occurs with basal nuclei lesion?

What occurs with basal nuclei lesion?

Direct - Indirect - Hyperdirect What are the three basal nuclei motor circuits? What are signs and symptoms of Huntington disease? (4) What is seen with motor damage in Huntington disease? Striatal damage can lead to: (3)

What are the three basal nuclei motor circuits?

Strong inhibition of movement What are two treatment options for Parkinson disease? The direct pathway: The indirect pathway: The hyperdirect pathway leads to:

The hyperdirect pathway leads to:

Week 12

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Medicine - Neurology

user_pereira_de_andr Created by 9 mon ago

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Movement selection and control - Regulation of muscle contraction, muscle force and sequencing of movements - Regulates which UMNs are to be excited and which need to inhibited to carry out desired movement and prevent unwanted movement - Initiation of movement/changing movement - Regulation of muscle tone

Imbalance of movement facilitation and inhibition

Direct - Indirect - Hyperdirect

More movement

Less movement

Strong inhibition of movement

Stops movements in progress

Facilitates specific desired movements

Prevents unwanted movements

Globus pallidus internus - Substantia nigra pars reticularis

The less overall movement there will be

Excitatory postsynaptic potentials - Inhibitory postsynaptic potentials

Glutamate

GABA

Inhibit the motor thalamus (ventral anterior and ventral lateral nuclei) - Inhibit the pedunculopontine nucleus (PPN) - Inhibit the midbrain locomotor region (MLR)

The ability of the thalamus to activate the motor cortices is reduced (decreased corticospinal and corticobrainstem activity)

The ability of the PPN to inhibit the medial reticulospinal tracts to the trunk and girdle muscles is reduced --> axial and girdle tone increases

The ability of the MLR to excite the medial reticulospinal tracts to activate SPGs is reduced --> decreased initiation and maintenance of gait

The VA and VL nuclei of the thalamus - The MLR - The PPN

Reduced movement - Increased axial tone - Reduced ambulation

The putamen - The output nuclei

Inhibit

Increased activity in corticospinal and corticobrainstem tracts - Decreased activity in medial reticulospinal tracts reducing trunk and girdle muscle tone - Increased activity in MLR increasing medial reticulospinal activation of SPGs for gait

Putamen - Output nuclei - Globus pallidus externus and the subthalamic nucleus

Inhibit - Inhibit - Excite - Disinhibited

Decreased activity of the corticospinal and corticobrainstem tracts - Increased activity of the medial reticulospinal tract leading to increased trunk and girdle tone - Decreased activity of the medial reticulospinal tract leading to decreased initiation and maintenance of gait

There is a very strong excitation of the STN by the cortex, leading to a large degree of excitation of the output nuclei

D1 and D2

Excite - Direct

Inhibit - Indirect

Facilitate activity in the motor cortices - Decrease activity in the medial reticulospinal tracts that modulate tone - Increase activity in the medial reticulospinal tracts that activate SPGs

Increases

Direct pathway - Dopamine

Indirect pathway - Output nuclei

Too much or too little movement

Constant, excessive, unregulated movement

Little movement

Decreased

Increased

Almost constant, rapid movements of the face, tongue or distal limbs

Slow, writhing movements often most pronounced in the hands

Wild, flailing movements or a constant rotary movement of one arm or leg

A lesion in the contralateral STN

Chorea - Athetosis - Choreoathetosis

Non-progressive movement disorder with sustained muscle contractions causing abnormal postures, twisting, and repetitive movements

Focal (localized)

Spasmotic torticollis

Genetic predisposition

Stress and activity

Sleep

Overactivity of the indirect pathway (somehow still a hyperkinetic disorder)

Genetic

All circuits affected with non-motor circuits typically affected prior to the motor circuit - Cell death in cortical neurons to striatum that progresses to the striatal neurons themselves

Personality behaviors (social behavior circuit) - Dementia (goal-directed behavior circuit) - Emotional dysregulation (emotion/motivation circuit) - Chorea (motor circuit)

Cell death, initially in striatal indirect pathway neurons (loss of GABAergic neurons to GPe) - Late in disease progresses to direct pathway

Decreased drive to move and decreased spontaneous movement

Dopaminergic cells in the substantia nigra pars compacta

Hypokinesia - Bradykinesia - Resting tremors (pill rolling) - Rigidity - Stooped posture - Loss of postural reflexes - Masked face - Gait disturbance

Movement and sleep - Stress

Slowness of movement

Non-velocity dependent

In the trunk compared to the extremities

Near normal

Plastic/lead pipe - Cog-wheel

Backwards

Impaired rhythmicity - Asymmetrically reduced arm swing - Narrow BOS - Difficulty initiating gait - Slow, short, shuffling steps - Freezing of gait (severe PD) - Festinating gait - Difficulty dual tasking while walking

Gait apraxia does not improve with auditory or visual cues, PD does - Gait apraxia has a wider BOS while PD has a narrow BOS - Gait apraxia symptoms are limited to walking, while individuals with PD have impaired LE function in/outside of weightbearing

Patients with gait apraxia have an erect posture - Gait apraxia is not associated with a resting tremor - Gait apraxia is not associated with rigidity - Gait apraxia does not improve with dopamine agonists

Dopamine agonists - Acetylcholine antagonists

Hyperkinesia

Dry everything

Exercise increases available dopamine to treat, slow down progression and improve patient status

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