Neuro

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-Controls muscle tone/glad secretion -Is usually excitatory but can be inhibitory (vagal response)

Acetylcholine

Neurotransmitters alllow for _____ of nerve conduction.

One-way and in one direction

-Controls mood, wakefulness, integration -Is excitatory (CV - Sympathetic)

Norepinephrine

-Controls mood, integration, and movement -Is inhibitory (r/t Parkinson’s)

Dopamine

-Controls wakefulness, sleep, mood, modulates pain -Is inhibitory

Serotonin

-Controls integration -Is excitatory (r/t seizure in TBI?)

Glutamate

-Controls integration -Is inhibitory

Glycine

-Controls wakefulness, awareness, integration -Is inhibitory

GABA

Includes - skin, periosteum, bone

Cranium

Includes - dura, arachnoid, and pia

Meninges

Includes - grey and white matter

Parenchyma

-Location: Cerebral Cortex -Function: behavior, personality, motor, smell -Sign of Injury/Lesion/Disorder: abnormal behavior

Frontal

-Location: Cerebral Cortex -Function: hearing, vision (crude), smell, taste -Sign of Injury/Lesion/Disorder: loss of hearing, crude vision, taste

Temporal

-Location: Cerebral Cortex -Function: language, motor, spatial/somatic experience -Sign of Injury/Lesion/Disorder: drawing objects, distinguishing left to right, spatial disorientation, problems reading and writing

Parietal

-Location: Cerebral Cortex -Function: vision and spatial orientation -Sign of Injury/Lesion/Disorder: visual hallucinations and field cut

Occipital

-Location: Cerebral Cortex -Function: sensory-speech -Sign of Injury/Lesion/Disorder: loss of sensation and speech problems

Wernicke’s Area

-Location: Cerebral Cortex -Function: motor-speech -Sign of Injury/Lesion/Disorder: movement and speech problems

Broca’s Area

-Location: Cerebral Cortex -Function: motor control (coordination) -Sign of Injury/Lesion/Disorder: balance problems, vision (nystagmus), speech problems, vertigo

Cerebellum

-Location: Mid-Brain -Function: Relays impulse to and from cerebral cortex, and controls consciousness -Sign of Injury/Lesion/Disorder: Decrease in LOC/loss of consciousness, memory loss, apathy

Thalamus

-Location: Mid-Brain -Function: regulates temperature, hungers, and hormones -Sign of Injury/Lesion/Disorder: metabolic, temperature regulation, extreme thirst or dehydration, weight loss or gain, high or low BP, frequent urination

Hypothalamus

-Location: Mid-Brain -Function: consciousness (sleep/wake cycles) -Sign of Injury/Lesion/Disorder: delirium, change in LOC

Reticular Activating System (RAS)

-Location: Mid-Brain -Function: motor control and tone (involuntary) -Sign of Injury/Lesion/Disorder: disordered muscle control and increased muscle tone

Basal Ganglia

-Location: Brain Stem -Function: nuclei for CN V-VII; nerves for head and neck -Sign of Injury/Lesion/Disorder: loss of sensation and motor, and difficulty with speech and swallowing

Pons

-Location: Brain Stem -Function: respiratory/vasomotor/cardiac control; nuclei for CN IX, X, XI, XII -Sign of Injury/Lesion/Disorder: breathing problems, problems swallowing/gag reflex, loss of muscle control and balance, uncontrollable hiccups

Medulla

-Feed from: Internal Carotid -Supplies blood to: Basal Ganglia, medial cerebral hemispheres, superior surface of frontal and parietal lobes -Symptoms of Injury: weakness and sensory loss of leg and foot opposite side of lesion

Anterior Cerebral Artery

-Feed from: Internal Carotid -Supplies blood to: frontal and parietal lobes, cortical surface of temporal lobe -Symptoms of Injury: paralysis, weakness, sensory loss to face and arm opposite lesion

Middle Cerebral Artery

-Feed from: Vetebral arteries -Supplies blood to: posterior cerebral hemispheres (occipital lobe) and brain stem -Symptoms of Injury: loss of consciousness, vision, coordination, and balance

Vetebral-Basilar Arteries

-Feed from: L and R common carotid, internal carotid, basilar artery -Supplies blood to: regulates differential blood flow to the brain

Circle of Willis

How is the BBB different from other capillaries in the body?

BBB is less permeable than other capillary beds, but permeable to water, CO2, O2, and slightly permeable to electrolytes, but impermeable to proteins and lipids

How is CSF produced and absorbed? What clinical manifestations could you see if CSF is not absorbed?

-Produced by the Carotid Plexus -Reabsorbed through the arachnoid villi -Caused a tremendous amount of salt loss-> Hyponatremia r/t Intraventricular Hemorrhage or an external shunt

Explain the components of cerebral hemodynamics and what the Monroe-Kellie Principle is.

-Manipulation of blood, CSF, and cerebral tissue/mass in the cerebral vault -As intracranial volume increases, ICP increases

Pathophysiology: compensated by controlling cerebral blood flow

Stage I

Manifestations: confusion, restlessness, lethargic Pathophysiology: early signs of elevated ICP

Stage II

Manifestations: hypoxia? hypercarbia, loss of autorregulation Pathophysiology: brain injury begins

Stage III

Pathophysiology: herniation of brain tissue from high to low pressure

Stage IV

Directly sends messages to organs (heart, lungs, muscles, etc)

SNS

Relaxes, uses ganglia to deliver messages to organs (indirectly)

Parasympathetic NS

Motor neurons -> carry motor stimuli to control skeletal muscles

Anterior Horn

Sensory neurons -> carry sensory signals to the brain

Posterior Horn

-Mylein develops into teen years making recovery easier (Plasciticy) -Reflexes are marker of healthy NS development -Normal reflexes change with age (1st year)

Children

-Decreaed neurons, myelin and dendrites process with synaptic connections (decrease brain weight and size) -Atherosclerosis -Increase BBB permeability -Functional changes (decrease deep tendon reflexes; decreased taste, smell, and color detection; sleep disturbances and memory impairment)

Elderly

-Etiology: genetic and environmental (triggers) -Manifestations: H/A for 4-72 hrs, unilateral or bilateral, (+/-) aura, no neuro deficits -> premonitory (presymptoms); migraine aura; headache; recovery (irrationally, fatigue, or depression) -Pathophysiology: unclear

Migraine HA

-Manifestations: unilateral, severe, stabbing and throbbing pain, sudden onset and short duration (1/2 hr) -> associated with ptosis, tearing, and nasal congestion -Common in men -Pathophysiology: r/t release of vasoactive peptides, neurogenic inflammation and pain activation

Cluster HA

-Etilogy: genetic?, episodic and chronic -Manifestations: bilateral pain (band, pressure), gradual onset -Pathophysiology: Central - trigeminal hypersensitivity; Peripheral- myofascial afferent sensitivity

Tension HA

-Pathophysiology: Inflammatory cytokines and medications (Benzos)-> disruption of neural network RAS; altered levels of neurotransmitters -Manifestations: acute confusion - acute onset with fluctuating cognitive impairment and varying states of awareness (2-3 days)

Delirium

-Pathophysiology: neuron degeneration, compression of brain tissue, vascular changes? -Manifestations: chronic onset with slow cognitive decline with no impairment of awareness, altered language and judgement

Dementia

-Etiology: genetics (APOE gene) and environment -Pathophysiology: loss of neurons and synapses in cerebral cortex and hippocampus (effects memory); Atrophy with decreased brain weight and size -> loss of neurotransmitters and generation -Manifestations: Early - autosomal dominant; Late - amyloid deposition, atherosclerosis, tangles , inflammation

Alzheimer’s

-Mode of Transmission: nasopharyngeal-> blood stream -> cross BBB -> meninges -Etiology: Nessiera Meningitis, S Pneumo, H Flu, Group B Strep -Manifestations: meningeal irritation -> nuccal rigidity (with projectile emesis when bending head), change in LOC, focal neurodeficits, seizures, rash, + Babinski, Labs -> CSF with high WBCs, + pmns, low glucose, high protein) -Pathophysiology: bacterial infection of meninges and paraenchyma

Bacterial Meningitis

-Etiology: mumps, herpes, Echovirus, influenza, Arbovirus -Manifestations: less severe than Bacterial Meningitis; HA, photophobia, mild neck pain, fever, malaise -Pathophysiology: limited to meninges themselves

Viral Meningitis

-Etiology: bites, HSV-1, herpes, West Nile, toxoplasmosis, cryptococcus (HIV), post-live vaccination, autoimmune (Lupus, RA) -Manifestations: significant neuro deficits -> meningitis -Pathophysiology: acute febrile illness with CNS (meningeal) involvement

Encephalitis

What are the common etiologies for seizures?

tumor, bleeding, trauma, biochemical alterations (hypoglycemia, hyponatremia, and hypernatremia), epilepsy (focal and generalized)

-Age: 6 mo - 5 yr -Duration: < 15 mins -Frequncy: 1 seizure in 24 hrs -Nature: generalized -Recovery: post-ictal with return to baseline and normal neuro exam

Simple Febrile Seizure

-Age: any age -Duration: >\= 15 mins -Frequncy: multi-seizures in 24 hrs -Nature: generalized or focal -Recovery: post-ictal, may not fully return to baseline after multiple seizures

Complex Febrile Seizures

Effects the same side of the body that seizure that is specific or complex (twitching or staring)

Focal

Effects entire body -> tonic/clonic and decreased LOC

Generalized

-Etiology: lack of dopamine -Pathophysiology: basal ganglia degeneration -> decreased dopamine-> Lewy Bodies-> further decrease dopamine -Manifestations: stooped, resting tremor, bradykinesia, rigidity, poor balance, postural instability, masked facies, flexed hips and knees

Parkinson’s

-Etiology: post-infectious (Mono?) -Pathophysiology: chronic inflammation and degradation of CNS myelin scarring, loss of axons (non-functional), fibrous gliosis -> white matter -Manifestations: parasthesia, weakness, poor gait, vision changes, urinary incontinence. commonly relapsing and remitting -> progressive.

Multiple Sclerosis

-Etiology: autoimmune associated with SLE, RA, thyroxicosis -Pathophysiology: defect in nerve impulse transmission at neuromuscular junction r/t acetylcholine receptor antibody -Manifestations: descending progressive paralysis and weakness

Myasthenia Gravis

-Etiology: post-infectious or post-immunization -Pathophysiology: humoral and cell-mediated reactions directed at peripheral nerves -Manifestations: ascending paralysis and weakness

Guillain Bare

-Etiology: prenatal, perinatal, postnatal -Pathophysiology: disorder of movement muscle tone and posture -Manifestations: permanent paralysis but not progressive

Cerebral Palsy

How do the 5 Ps play a role in strokes?

Parenchyma- what part of the brain impacted? Pipes- blood vessels, which ones involved? Perfusion- restoring as much as we can Penumbra- cells around infarct that survive are at risk Prevent Complications- early intervention and stroke management

-Deficits sudden -Most common is unilateral weakness and limb parathesia -Resolves < 60 mins -No evidence of infarct but increased risk of stroke in 3 months

TIA

-Deficits sudden -Reversible >/= 24 hrs

Reversible Ischemic Neuro Deficit

-Deficit progress 24-36 hrs -Motor hemipalegia, hemisensory, dysarthria, ataxia -Small lesions in penetrating arteries linked to vascular dementia

Lacunar Stroke

-Etiology: Atherosclerosis and inflammation (common) -Manifestations: deficits progress over time -Pathophysiology: usually large vessel

Thrombotic Stroke

-Etiology: Afib, patent foramen ovalvae, air, bacterial (valve veg), or fat embolus, tumors -Manifestations: deficit worse at onset common in MCA -Pathophysiology: common in MCA

Embolic Stroke

-Etiology: aneurysms -Manifestations: sudden and progressive symptoms; bleeding between arachnoid spaces and pia matter -Pathophysiology: AVM rupture

SAH

-Etiology: HTN, anticoagulants -Manifestations: sudden onset and progress rapidly -Pathophysiology: bleeding in parenchyma, basal ganglia, and putamen (common)

Intracerebral Hemorrhage

Dura intact (no visible brain)

Closed TBI

Skull fracture and break in dura (exposed brain)

Open TBI

Localized-Direct impact (more deadly) -> scalp laceration, skull fracture, contusion, hemorrhage

Focal TBI

Affects all areas of the brain (more long term complications): Acceleration/deceleration rationale -> contusion, diffuse axonal injury

Diffuse TBI

-Etiology: skull fracture -Manifestations: acute -> rapid loss of consciousness; Biconvex shape on CT -Pathophysiology: tearing of middle meningeal artery blood between dura and skull

Epidural Hemorrhage

Manifestations: symptoms depend on severity. Usually crescent shape on CT. Pathophysiology: bleeding between dura and arachnoid matter, tear in bridging veins

SDH

-Etiology: trauma, stroke, tumor -Pathophysiology: blood in parenchyma and ventricles

Intracerebral Hemorrhage

-Etiology: Aneurysm rupture or sheering injuries -Pathophysiology: bleeding between arachnoid and pia; blood in Circle of Willis, Cisterns and Fissures

SAH

What causes diffuse axonal injury and how does it manifest?

-Sheering and stretching of axons -> sheer off dendrites -Not associated with increased ICP -Severity depends on location and amount of sheering force

Pathophysiology: alternations of brain function caused by external force (falls, MVC, etc)

Primary Brain Injury

How do you prevent secondary brain injury?

Manage: hypotension, hyperthermia, hypoglycemia, hypercarbia, and hyponatremia

-Etiology: occurs with mild TBI -Manifestations: HA, dizziness, anxiety, irritability, photophobia, insomnia, despression, decreaed concentration

Post-Concussive Syndrome

-Etiology: TBI r/t sports, blast injuries, etc -Pathophysiology: progressive dementia and neurofibrillary tangles -Manifestations: violent loss of control, depression, suicide, memory loss, cognitive loss

Chronic Traumatic Brain Injury

Describe the mechanisms for sustaining a spinal cord injury

-mechanical trauma and immediate tissue injury (or if not properly immobilized) -caused by flexion, extension, compression, or rotation

temporary disruption of cord function

cord concussion

Bruising of neural tissue causing swelling and temporary loss of function

Cord Contusion

Pressure on cord causing ischemia

Cord Compression

Tear of tissue of cord

Cord Laceration

Severing the cord

Cord Transection

What are the key levels in spinal cord injury to maintain function?

-Quad >/= C6 -Para with arms >/= T6 -Para with trunk </= L1

Explain the components of cerebral hemodynamics and what the Monroe-Kellie Principle is.

-Manipulation of blood, CSF, and cerebral tissue/mass in the cerebral vault -As intracranial volume increases, ICP increases

Strokes affecting vision and sensory are associated with?

MCA

Strokes affecting vision and depth perception are associated with?

Posterior Cerebral Artery

Strokes affecting swallowing, speech, pain, temperature, muscle strength, gait, and balance are associated with?

Vertebral Artery

Right sided brain injury causes?

-Paralysis on L side -Spatial/perceptual deficits -Impulsive behavior -Memory deficits

Left sided brain injuries cause?

-Paralyzed R side -Speech/language deficits -Slow/cautious behavior -Memory deficits

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