Clinical Neuroscience - Neurorehabilitation

Wichtige Krankheitsbilder der Neurowissenschaften - Neurorehabilitation

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This flashcard set delves into the complexities of neurorehabilitation, focusing on motor learning, spinal cord injury, and stroke recovery. It covers key aspects like myelin repair, compensatory and regenerative sprouting, and the phases of damage following trauma. The set is tailored for university-level students in medical fields, offering insights into novel therapy approaches and the structural and functional repairs post-CNS trauma. It benefits those seeking a deeper understanding of rehabilitation mechanisms and the latest advancements in treating neurological impairments.

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After physical trauma (spinal cord injury) 3 phases of damage occur. Which one?

primary phase: immediate damage

secondary phase: degenerative events)

late phase

intermediate pahse

Primary phase is the immediate destruction of tissue by necrosis. Which are the secondary degenerative events which are mediated by different mechanims?

ISCHEMIA (in surrounding tissue); vessels: slow ischemic death of neurons

RELEASE of neurotransmitters from ischemic terminals neurons (toxic intracellular Ca2+)

FREE RADICAL formation (due to iron from bleeding)

inflammation, meylin damage and prsseure damage (from edema)

DEMYELINATION

What are the events of the late phase?

SCARE formation

by astrocytes, microglia/macrophages and menigeal fibroblast

CYST formation

cysts are filled with Cerebrospinal fluid

LESION

Stroke (ischemic lesion) is not the same as a traumatic injury. Which are the most important events of strokes?

death of tissue (necrosis) in center of lesion

slower degenerative processes in surrounding tissue

surrounding is called 'penumbra'

late phase: fluid filled 'holes' surrounded by scar

inflammation

Neuroprotection is a way to reduce impacts of secondary phase injury. Which are the positive measures taken (all have only minor effect!)?

HYPOTHERMIA effective in brain/stroke but not in spinal cord

Animal model: radical scavenger, Glu-receptor & CA2+-channel blockers, negative in brain

ANTI-edema and ANTI-inflammatory (brain & spinal cord)

decompression and spinal cord stabilization only in spinal cord

Animal model: myelin repair

Which are the functional consequences of lesions?

Paraplegia: paralysis of legs and lower body

injury of lumbar or thoracic spinal cord leads to paraplegia

Tetraplegia: paralysis of upper and lower extremities

injury of cervical spinal cord leads to tetraplegia

Hemiplegia/Hemiparesis: impairment of one side after stroke (unilateral)

What are the structural and functional repairs after CNS trauma?

Regenerative sprouting and elongation (injured axons)

Compensatory sprouting (intact fibers)

map shifts

new neurons or oligodendrocytes

formation of new axons/neurons

What is true about regenerative sprouting?

sprouts are reactions to injury trying for a transitory regeneration

sprouts can connect to targets proximal to the lesion

contact spared propriospinal neurons (‘relay pathway’)

Regeneration can be stimulated (antibodies against growth factors)

NogoA is not an example for such ABs

What is true about compensatory sprouting?

Intact fibers sprout and take over targets that have lost their input

formation a new functional circuit

formation leads to a 'remapping'

remapping = map shifts

fibers can overtake complete loss of function

What is true about myelin repair?

myelin repair = formation of new myeoin or oligodendrocytes

frequently: proliferation of stem cells in surrounding trauma site

new neurons are present

astrocytes contribute to scar fomation

some cells (10%) differentiate into oligodendrocytes --> myelin

What are the known facts about motor learning?

improvement is dependent on amount of practice

task variability improves performance after impairment

sporadic feedback after delay is superior to consistent feedback

greater retention/transfer with random practice

better movement quality with whole-task practice

What is true about stroke and recovery?

ca. 10 million strokes per year

80% with motor deficits

10-90% with sensory deficits

poor functional recovery with persistent/severe sensory deficits

conventional rehabilitation focuses on visually guided motor training

Motor relearning in hemiparesis: there are only a few studies about this topic. Conventional rehabilitation seems to no/little effect on impairment. The CIMT - Constraint-induced Movement Therapy - seems to be the best way to achieve some recovery. What is true about CIMT?

effect is scientifically proven but it is a frustrating procedure

the less effected extremity is restraint for 90% working hours

the affected limb is trained 6h/day (=forced use)

also possible in patients with no motor function

not clear: impairment reduction of compensatory strategy?

What are the most important novel therapy approaches?

technology-based assesments (e.g. Peg insertion)

robot-assisted rehabilitation (FES, ...)

neural stimulation (brain stimulation = TMS or tDCS)

brain-machine interfaces (MEG, EEG, fNIRS)

drugs

Conclusion of Rehabilitation therapy in storke/spinal cord injury?

robot-assisted therapy is good but not better than personell

problem: lack in understanding recovery mechanisms and lack in tools for understanding

Promote close collaboration between scientists, clinicians and engineers

Promote motor learning for novel therapies: mainly treat sensory AND motor aspects

no interaction dynamics and brain loop

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Clinical Neuroscience - Neurorehabilitation

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