CNS disorders Flashcards
what are the two main sources of blood into the circle of willis
- internal carotid
- vertebral artery
ACA- anterior cerebral artery
- branches from internal carotid
- had many superficial and deep branches and anastomosis
MCA - middle cerebral artery
- branches from internal carotid
- 4 main branches
PCA - posterior cerebral artery
- branch from the basilar artery near the pituitary stalk at the ponotmesencephalic junction
supplies
- occipital lobe,
- inferomedial temporal lobe,
- a large portion of the thalamus
- upper brain stem,
- midbrain,
- lateral geniculate body
- hippocampus
- parahyippocampal gryus
CNS cells:
- neurons
- macroglia:
- microglia
What are macroglia and describe
derived from nerve cell linage
- astrocytes: provide structure
- oligodendrocytes: myleinate
- Schwann: mylinate in PNS
- ependymal cells: help produce CSF
Microglia
- derived from monocyte cell lineage
- immune cell of brain
- 10% of CNS cells
- clean foreign bodies
- are times where microglia stay active and cause damage
Cellular dysfunction: neural cell death
- apoptosis: programmed but can cause damage if it outside normal range of occurring
- necrosis: unplanned usually caused by an external factor, cell membrane gets disrupted and the insides affect other cells when they leak out
Cellular dysfunction: excitotoxicity
- free radicals: can be dangerous or harmful
- released during exercise but that helps the body understand how to deal with them
What regulates the extracellular environment of the CNS
- blood brain barrier: tightly joined endothelial cells; block diffusion
- ependymal cells: line ventricles and spinal canal and regulate metabolism
- regulate the extracellular environment and protect the nervous system structures
Amino acid Neurotransmitters
- glutamate: excitation
- GABA & Glycine: inhibitory
Amines Neurotransmitters
- cholinergic = acetylcholine
- biogenic: catecholamines, serotonin
- neuopeptides Neurotransmitters
- enkephalins
- b-endorphins
- substance P
gaseous Neurotransmitters
- nitrous oxide NO
Sympathetic NS neurotransmitters and what they cause as well as receptor types
- adrenergic stimulate sympathetic NS
- can have a positive effect meaning it increases sympathetic response or a negative effect meaning that it decreases sympathetic response
- receptor types: alpha and beta
- nicotinic receptor at preganglioic neuron
parasympathetic Neurotransmitters
- cholinergics for both pre and post ganglionic
- only positive effects
- adrenergics
- cholinergincs
- stimulate sympathetic NS
- stimulate parasympatheic NS
beta blockers
vs
alpha blockers
- inhibit sympathetic (beta receptors mostly)
- inhibit sympathetic (alpha receptors mostly)
anticholinergics
inhibit parasympathetic NS
what are side effects of increase in parasympathetic function
- GI distress: nausea, vomiting, diarrhea,
- abdominal cramping,
- bronchoconstriction,
- increase salivation
- bradycardia
- pupils constricted
- impacts vision
Biogenic amines
- norepinephrine
- Dopamine
- serotonin
- work together to regulate attention and alertness
Norepinephrine effects with Mental health regulation
- attention
- motivation
- pleasure
- reward
- mood
Dopamine
- alertness
- energy
- Anxiety
- involved in movement quality
Serotonin
- obsession
- compulsions
CNS disorders
Infections
neoplasm
vascular
trauma
degenerative
Infectious disorders of the CNS
- Meningitis (viral, tuberculous, bacterial)
- encephalitis
- brain abscess
Neoplasms
- tumor
Vascular- CNS disorder
TIA
stroke
Trauma- CNS disorder
TBI
Degenerative disorders - CNS disorders
- get progressively worse
- ALS
- Alzheimer’s
- huntington disease
- MS
- Parkinson
Examples of the variety of clinical manifestations of CNS disorders
- Sensory disturbances
- Movement disorders
- disorders of coordination movement
- deficits of higher brain function
- altered states of consciousness
- emotional instability
- memory problems
- brainstem dysfunction
- autonomic system dysfunction
- aging and the CNS
Sensory disturbances: spinal cord lesion
- decreased pain on CL side and decreased touch on ipsilateral side
Lesion above medulla
- decreased pain and touch on contralateral side
Spinal cord lesions DCML
- sensations ipsilateral deficits
Anterolateral spinal cord lesions
- contralateral deficits
Motor system pathways
- Anterior corticospinal tract
- lateral cortiocospinal
Hypotonicity vs hypertonicity
describing resting tone
Spasticity
- type of hypertonia that is velocity dependent
Dysmetria
- dysfunction with moving certain distance
- proximation
Dysdiadochokinesia
-Inability to preform rapid reciprocal movement
- coordination
Ataxia vs apraxia
- (1). Difficulty controlling movement
- (2). difficulty initiating movement
Gaze-evoked nystagmus
- eyes don’t stop after rapid head movement don’t stop once head stops
- Aphasia
- Agnosia
- dysarthria
- anarthria
- trouble with expression and reception of language
- unable to recognize objects/people
- trouble generating speech
- without speech
Higher brain function deficits in CNS disorders
- language vs speech
- perception
- abstract thinking
- movement
- adaptive response
- frontal lobe damage
- right hemisphere syndrome
- Alexia: difficulty with reading
Disorders of consciousness and emotion
- Reticular activating system: arousal and attention
- orbital prefrontal region: selective attention to facial expression
- limbic system: orbitofrontal cortex, hippocampus, parahippocampal gyrus, cingulate gyrus, cingulate gyrus,hippocampus
- amygdala: integrates emotion and context in stress response
Diagnosis of CNS disorders
- clinical localization
- computed tomography
- MRI: typical first done
- fMRI
- PET
- DaTSCAN
- Diffusion Tensor imaging
- EEG
- Brainstem auditory evoked potentials
- transcranial doppler ultrasound
- near-infrared spectroscopy
- transcranial magnetic stimulate
Treatment for CNS disorders
Pharmacologic:
- modulate neurotransmitter synthesis, release, reuptake or degradation (can be used to enhanced movement not just mental health)
- antioxidant therapies to prevent free radicals from penetrating membrane
- pharmacology for movement disorders
- antipsychotic and antidepressants
- opioid analgesics
Stem cells
Meningitis
- inflammation
- viral aseptic infection vs bacterial infection
Meningitis: risk factors
- immunodeficiency
- crowded living spaces
- spleen dysfunction
Pathogenesis of bacterial meningitis
- depends on insulting agent
- typicall gets into the blood stream and can go throug BBB by way of a WBC
Clinical manifestations: meningitis
Also what is the only way to diangosis
- cardinal signs: headache
- stiff neck
- non-balancing rash
- septicemia
- red flags signs: cold hands/feet, limb pain; pale mottled skin
- nausea and vomiting
- lumbar puncture= spinal tap for diagnosis
Treatment: meningitis
- bacterial Meningitis: antimicrobials and steroids
- viral meningitis
Encephalitis:
- acute inflammatory disease of the parenchyma or tissue of the brain
causes of encephalitis
- direct viral invasion or hypersensitivity initiated by a virus herpes simplex virus
- autoimmune
- bacterial
- insects bites
Pathogenesis of encephalitis
- destruction of cell membrane
- gliosis and scarring
- white matter destruction
Clinical manifestations: encephalitis
- headahce, weakness, UMN signs
- can combine with meningitis and become meningoencephalitis
- altered mental status
- movement disorders
- ataxia
- cranial nerve defects
Medical management: encephalitis
Diagnosis, treament,
- Dx: IgM antibodies in serum or CSF
- Treatment: varies with the infectious agent; antiviral if causes by herpes simplex virus
Brain abscess
- uncommon
- focal infection
brain abscess: risk factors
- compromised immune system receiving steroid
- immunosuppressants or cytotoxic chemotherapy
- systemic illness such as HIV infections
Clinical manifestations; brain abscess
- headache, disturbed consciousness, and fever
Zika
- RNA virus transmitted by specific mosquito bite
- usually asymptomatic
- fever, rash, jt pain, conjunctivitis
- affects fetus
- Prions disease
- genetic or acquired
- creutzfeld-joakob disease
- 50-80 years old
- cognitive impairment/confusion/movement disorders
- fatal
Degenerative CNS disorders
- ALS - amyotrophic lateral scleosis
- dementia
- huntington disease
- MS
- parkinson
ALS: classifications
- pseudobulbar
- progressive bulbar palsy
- primary lateral sclerosis
- progressive spinal muscular atrophy
*bulbar = cranial nerve
ALS symtpoms
- depend on whether it is UMN or LMN
- typically musucle weakness and atrophy
- extremities affected first with progression to respiratory muscles
Types of dementia
- alzheimers disease
- lewy body dementia
- vascular dementia
- Frontotemportal disorder
Dementia
Alzheimers disease
- memory loss
- language problems
- unpredictable behavior
- amyloid plaques
- tau tangles
Dementia
Lewy Body Dementia
- difficulty with thinkng, movement, behavior, mood
- abnormal deposits of a protein (alpha-synuclein)
- affects acetylcholine and dopamine in the brain
Dementia
- Vascular dementia
- disruption in blood flow
Dementia
Frontotemporal disorder
- when nerve cells in the frontal and temporal lobes of the brain are lost
- behaviors
- emotions
- communication
- walking
- rare and affects younger people (45-64)
Huntington disease
- progressive genetic disorder
- usually beginning in 30s-40s
huntington’s disease
signs and symtoms
- movement: choreic movement (ataxic) and rigid/difficulty moving
- cognition: may be detected before motor deficits
- psychiatric disorders
- atrophy of caudate nucleus and putamen of basal ganglia
- white matter deterioation in frontal lobe
Multiple sclerosis
-what causes it, what occurs, when is it dx, and risk facotrs
- scleotic plaques throught the brain and spinal cord
- inflammation, demyleination, axon loss and gliosis
- typically dx between 20-50 years
- infection from epstein-barr, herpes, immune response, environment, genetics
Symptoms of MS`
- sensory
- motor
- bowel
- bladder
- affect
- coordintion
Treatment of MS
- disease modifying agents
- immunomodulating/immunosupressives
- monoclonal antibodies
- steriods
Parkinson disease
- degeneration of basal ganglia neurons
- stop producing dopamine (symptoms occur when it is down 70-80%)
- disrupts communication with cortex
- chronic, progresisve disease
hallmark traits of parkinsons
- rigidity
- tremor
- bradykinesia
- postural instability
risk factors for parkinsons
- genetic
- toxic or infectious exposures
