9/29 Motor Control Lesions

Question 1

Recognize and define different terms to describe paralysis and weakness

Answer 1

• Paresis—weakness (partial paralysis). -plegia—no movement. Paralysis—no movement. Palsy—imprecise weakness/no movement.
• Hemi-one side of body. Para—both legs. Mono—one limb. Di—both sides of body. Quadri/tetra- all four limbs.

Question 2

• Be able to define upper (UMN) and lower motor neuron (LMN). Be able to identify the different symptoms caused by UMN and LMN lesions

Answer 2

• UMN—neuron from motor cortex to ventral spinal cord. LMN—neuron from ventral spinal cord to muscle.
• Weakness can be caused by upper or lower. Atrophy and fasciculations only lower. Reflexes and tone are increased with UMR lesions decreased with LMR lesions.

Question 3

• Be able to explain the difference between areflexia and hyperreflexia and their causes.

Answer 3

• Areflexia is no reflexes and is caused by lesions of LMN. Hyperreflexia is too strong a reflex caused by UMN lesions because inhibition from the cortex is removed.

Question 4

• Describe the babinsi test for corticospinal function

Answer 4

• A Babinski sign occurs when the corticospinal tract is no longer influencing reflexes in the feet. Leads to spread toes rather than curled. The problem is somewhere between the primary motor cortex and lumbar spinal cord.

Question 5

Be able to locate lesions in the nervous system that cause arm motor deficits.

Answer 5

• Lesions in the arm region of the cortex (contralateral), internal capsule/cerebral peduncle (contralateral), LMN lesions in nerve. Cervical cord lesions that affect entire ventral cord (ventral horns): bilateral arm, CST spared; nerve lesion—atrophy and areflexia.

Question 6

• Be able to locate lesions in the nervous system that cause leg motor deficits.

Answer 6

• Lesions in internal capsule/cerebral peduncle (contralateral), lesions to medial cortex (leg region of BA4) (contralateral). UMN lesions in CST above cervical cord affect leg function. LMN lesion in nerve.

Question 7

• Be able to locate lesions in the nervous system that cause face paralysis.

Answer 7

• Bottom face: lesions in the face region of the cortex (contralateral), Lesions in internal capsule (genu) (contralateral). Entire face: lower motor neuron lesion (ipsilateral)

Question 8

• Be able to describe the general reason that unilateral cortical lesions do not cause paralysis of the upper face.

Answer 8

• Because the cortical pathway responsible for moving the upper face is bilateral

Question 9

• Be able to locate lesions in the nervous system that simultaneously cause motor deficits to the body below the face.

Answer 9

• Lesions in the BA4 not including face region or in medulla/cervical cord.

Question 10

• Rubrospinal tract lesions

Answer 10

• Flexor bias. Kept in check by cortical control. Lesion above red nucleus=loss of cortical control extreme flexion/decorticate. Lesion below red nucleus=loss of outputloss of flexion/decerebrate.

Question 11

• Define Amyotrophic Lateral Sclerosis

Answer 11

• ALS: affects nerve cells responsible for voluntary movement. Link between brain and voluntary muscles upper and lower motor neurons degenerate and die. Muscles degenerate cannot function. Most die of respiratory failure

Question 12

• Be able to define the basal ganglia loop changes that occur in PD

Answer 12

• Decreased DA from the substantia nigra leads to increased D2 loss of excitation in indirect pathway of GPe by putamen resulting in decreased inhibitory output from GPe to STN. This decreased inhibitory output leads to excessive excitatory output to the GPi increasing inhibitory output of GPi to thalamus and brainstem. Both the direct and indirect pathways lead to increased inhibitory activity from GPi to the thalamus and brainstem

Question 13

• Describe the characteristics of basal ganglia diseases

Answer 13

• Tremor and involuntary movements, changes in posture and muscle tone, slowness without paralysis. Excess or diminished movement. Cognitive changes via dorsal caudate nucleus. Not Huntington’s

Question 14

• Be able to describe why DBS/pallidotomy is effective in PD for motor symptoms using BG circuits

Answer 14

• Pallidotomy (GPi ablation) is therapeutic because the GPi is overactive in the presence of reduced DA. Destruction of the nucleus should return activity in downstream nuclei to normal levels.

Question 15

• Be able to describe the neuropathology and symptoms of Huntington’s disease

Answer 15

• Chorea (dance like movements, semipurposeful) parkinsomism in juveniles, motor inpersistence, eye movement abnormalities, neurobehavioral symptoms (instability depression), dementia

Question 16

• Be able to discuss HD in context of BG pathways

Answer 16

• Neuronal loss, gliosiscaudate atrophy and cortical thinning. Genetically caused by AD, CAG repeat, and Chr 4, 100% penetrance, by 29-35, definite by 36. Used to think striatal neurons died which would result in reduced GPi output increased cortical drive. But, people are in a vegetative state towards the end, there is no DBS treatment for HD.

Question 17

• Be able to describe the functional consequences of cerebellar lesions

Answer 17

Ataxia is ipsilateral to side of lesion via crossed dentatothalamic path and crossed corticospinals (cross then recross), Midline lesions of vermis or flocculonodular lobe cause unsteady gait and eye movement abnormalities accompanied by intense vertigo, lesions to lateral vermis cause ataxia of limbs, deterioration of coordinated movement. Timing delays, hands. Dysmetria=overshooting, hypermetria=undershooting, hypometria= spatial target dysarthic speech—slurred, slow

Question 18

• Be able to describe the acute and chronic effects of ethanol on the cerebellum

Answer 18

• All along midline of forebrain and cerebellum (vermis). Anterior vermis loss of Purkinje and granule cells with white matter degeneration. Loss of ability to perform hell to toe test, increased GABA release from Purkinje cells, can be from fetal alcohol syndrome