Intro to CNS Disorders Study Guide PDF

Intro to CNS disorders study guide Disruption in neurons may result in: – Abnormal perception of environment – Uncoordinated movement – Loss of muscle force production – Impaired cognition/expression Necrosis- have internal cellular swelling, cell membrane ruptures, fragmentation, cell...

Intro to CNS disorders study guide Disruption in neurons may result in: – Abnormal perception of environment – Uncoordinated movement – Loss of muscle force production – Impaired cognition/expression Necrosis- have internal cellular swelling, cell membrane ruptures, fragmentation, cell disintegration Apoptosis-programmed cell death, no inflammatory response, DNA degradation, fragmentation Age Related Changes to CNS: -Loss of brain tissue → ↓ brain wt. with age -↓ nerve conduction velocity -Presence of lipofuscin in cell cytoplasm -Plaques of amyloid B protein in cerebral cortex -Neuritic plaques (associated with dementia and Alzheimer’s disease) -Neurofibrillary tangles (associated with Alzheimer’s disease) -Decreased glucose to the brain -Decrease in synthesis of neurotransmitter and # of receptors -Loss of myelinated nerves to vestibular system -Vision and somatosensory changes -Generalized loss of “functional reserve” Glial cells (supportive cells) Astrocytes Oligodendrocytes Schwann cells -most numerous cells in brain -Produce myelin sheath -Produce myelin sheath -Connect to capillary wall AND around axons in CNS around axons of PNS nerve cells → -Dysfunction of these cells -Recall: neuronal damage in supportive/nutritional function seen in demyelinating PNS are reversible Functions: diseases like MS Permeable to K+, maintain ion balance Monitor extracellular glutamate and remove/release it  Remove excessive glutamate and debris after injury -Astrocyte swelling common after injury, can lead to “scarring”, can compress surrounding neurons → tumors Neurotransmitters Name Action Related pathology Glutamate Excitatory -Excess levels seen after stroke, brain, spinal cord injury -Genes may trigger release of excess glutamate in ALS, Huntington’s, Alzheimer’s, Parkinson’s Disease Acetylcholine Excitatory or Inhibitory -Decreased production seen with Alzheimer’s disease Dopamine Usually excitatory -Decreased levels seen with Parkinsonism Norepinephrine Usually excitatory -Overstimulation can be result of cocaine or amphetamine overdose Serotonin Inhibitory -Involved with control of mood and anxiety GABA Inhibitory -Increased GABA activity decreases seizure activity Pathways Sensory Motor Bulbar DCML: Light touch and -Lateral corticospinal tract: Mostly bilateral with some proprioception Pyramidal decussation, exceptions Spinothalamic: Pain and temp contralateral, motor neurons of limb muscles -Ventral corticospinal tract: Descends ipsilaterally, terminates bilaterally to motor neurons of axial/trunk muscles Cerebellar Dysfunction Ataxia Incoordination of movement Dysmetria -Under or overestimation of necessary movement towards a target -Intention tremors with movement seen as overshoot and undershoot Dysdiadochokinesia Inability to perform rapidly alternating movement Scanning speech -Selection of words not affected -Words pronounced slowly and without melody, tone motor Infectious CNS Diseases Meningitis Encephalitis Brain abscess Prion disease Viral, bacterial, Acute inflammation -Local infection by -“prion protein” is tuberculous of brain tissue bacteria, fungi, causative -Fever, HA, stiff -Viral infection (west parasites agent-trigger normal painful neck nile virus) -Common with pts protein in the brain to - + Brudzinski’s, -HA, nausea, receiving steroids, fold abnormally Kernig’s signs vomiting, malaise chemo, etc. -Most common form -Body temp and of prion disease that white cell counts affects humans is often elevated Creutzfeldt-Jakob -HA, seizures, disease confusion -Slow incubation (5-8 -Potential symptoms years) of space occupying -Ataxia, lesion (eg tumor), incoordination, ICP symptoms dementia, sleep/wake cycle changes -Rare, fatal and  neurodegenerative disease with a long asymptomatic latent period Multiple Sclerosis: - Sclerotic plaques in CNS slow or block neural transmission and affects multiple body systems -4 subtypes: Relapsing-remitting (most common), secondary progressive, primary progressive and progressing-relapsing (rarest form) -HLA (Human Leukocyte Antigen) on chromosome 6 has been identified as genetic determinant in some cases of MS -Primary demyelinating disorder -Optic neuritis often the first clinical sign leading to visual disturbances -Sensory changes (Visual blurring, diplopia, weakness, balance problems, paresthesias and loss of discriminative touch (DCML)) -Motor changes (fatigue, spasticity & weakness) -Changes at brainstem level (trigeminal neuralgia, facial weakness, dysarthria, dysphagia and gaze palsies) -Other symptoms: ataxia, pain (neuropathic - up to 50% of cases), depression and bowel/bladder dysfunction (spinal cord involvement) -Treatment: use of immunosuppressive meds and meds for symptomatic relief → muscle relaxers, antidepressants, sleep meds, corticosteroids -PT implications: maintenance of function in household and community a primary goal and avoiding exhaustion, energy conservation strategies important