Patho Exam 5

Intracranial Pressure (ICP)

-average pressure inside the skull

-normall 5-15 mmHg for adults

-Regulating ICP

• Monroe-Kellie Hypothesis- body compensates to keep in range for ICp pressure (balance volume between):

  • brain tissue- remains relatively stable

  • CSF

  • Blood

Increased ICP

-etiology

• cerebeal edema (sodium)

• cerebral hemorrhage

• space-occupying lesions- tumor, abscess

• hypoxia, hypercapnia- cerebral vasodilation (increase blood supply)

-manifestations

• altered mental status (most common)

• nausea, vomiting

• headache

• sluggish pupillary reaction, papilledema (vision changes)

• seizures

-late stage manifestations

• Cushing’s Triad- decreased HR, irregular respirations, increased pulse pressure

• final stage coma

Posturing

-decorticate posturing- damage to corticospinal tract

• in response to stimulation, extend legs and pull arms into their core

-decerebrate posturing- upper brain stem damage

• in response to stimuli, extends legs and arms

Traumatic Brain Injury

-etiology

• blunt trauma

• acceleration/decelleration (brain tissue hits front, then back of skull- coup and contre coup injury)

• penetrating injury

• blast injury

Concussion

-physiological disruption in brain function caused by traumatic forces

-pathophysiology

• head trauma → abnormal metabolic function (stress on cells) → glutamate release → increase cellular permeability → Na/H2O surge into cells → temporary neuronal swelling

-manifestations

• alteration in conciousness

• headache

• dizziness

• double vision

• amnesia

• post concussion syndrome if symptoms last > 3 weeks

-Red Flag Concussion Symptoms

• worsening headache that will not go awat

• increased confusion, unusual behavior, restless, deterioating mental state

• slurred sppech, numbness, decrease in coordination

• drowsiness (loss of conciousness, won’t wake up)

• repeated vomiting, nausea, seizures

• one pupil larger than the other

Diffuse Axonal Injury

-widespread damage of tissue- white matter (axons)

• damage to axon itself as they twist, pull away from juncture, and possibly break

• more serious than concussion

-start with mild headache/confusion → progress to loss of conciousness

Cerebral Contusion

-bruise of brain tissue

-pathophysiology

• impact → microvascular damage → bleeding into tissues → inflammation and edema → increased ICP → cellular damge → increased risk for hernitation

-early manifestations

• dissiness

• severe headache

• vomiting

• unequal pupils

• unilateral weakness

-late stage manifestations

• lethargy

• confusion

• Cushing’s Triad- bradycardia, bradypnea, HTN

Subdural Hematoma

-bleeding that accumulates in between the dura mater and arachnoid membrane (subdural space)

-tearing of veins in subdural space → slow venous bleed

• venous bleed usually (slower, spreads out more)

• blood isn’t restricted by sutures → distributed over larger area (less compression of tissue)

Epidural Hematoma

-bleed in the space below the skull bone and above the dura mater

• stuck in suture areas → blood cannot spread around skull → ICP build up with increase in hematoma size → worsening of symptoms

• most likely arterial bleed (increases ICP more rapidly)

-quickly increases ICP and pushes cerebral tissue out of area

• herniation called midline shift- bows away from hematoma location

Hematoma (epidural and subdural) Manifestations

-headaches

-seizures

-vomiting

-focal neurological sypmtoms

-vomiting

-fixed dilated pupil

-signs of increased ICP

• Cushing’s Triad- bradycardia, irregular respirations, widening pulse pressure

Subarachnoid Hemorrhage

-bleeding within the subarachmoid space of the brain

• between the pia mater and the arachnoid membrane

• rapid, large amounts of blood released into subrachnoid space

-traumatic- cerebral/meningeal vessel tearing

-aneurysmal- rupture of cerebral aneurysms

-manifestations

• sudden, severe ‘thunderclap’ headache

• decreased level of conciousness

• neck stiffness

• vision changes

• seizures

Spinal Cord Injury (SCI)

-injury to the spinal cord leading to temporary or permanent loss of sensory, motor, and/or autonomic function

• hyperflexion

• penetrating

• rotation

• hyperextension

• vertical compression

-primary injury- actual harm to spinal cord

• sudden, traumatic injury on spine to fracture/dislocate vertebrae (compression of cord)

-secondary injury- comes from the body’s response to initial injury

• bleeding, inflammation, swelling that worsen SCI by damaging neuronal cells

-Types of Injury

• complete- destruction of function below point of injury

• incomplete- only lose partial function of spinal cord

• if at/above C4 level- loose diaphragmatic control

  • damage to this area must have respiratory support as they lose autonomic innervation of their diaphragm

Skull Fractures

-CAT scan to check for fractures (types)

• diastatic- usually found around lines of sutures

• depressed- depression in skull (spider-web looking)

• linear- cracks

• basilar- fracture close to base of skull

  • super worrisome- associated with fractures of other small bones, increased risk for leakage of CSF bc of close to brain stem and spinal cords

-manifestations

• Raccoon Eyes

• Battle’s sign

Meningitis

-inflammation of the meninges

-nasopharynx into bloodstream → subarachnoid space → blood brain barrier → organisms into CSF and meninges

• blood translocates into meningies (bacterial often)

-manifestations

• main: headache, fever, photophobia, Nuchal (neck) rigidity

• others:

  • Kernig sign (resistance to extension of the leg when straightened

  • Brudzinski sign- when neck is flexed by provider → leg flexes

  • MS changes

  • seizures

Encephalitis

-inflammation of the brain tissue

-etiology

• bacterial

• fungal

• parasitic

• autoimmune

• build up of ammonia

-manifestations

• fever, fatigue, headache

• increased ICp signs: vomiting, Cushing’s Triad

• meningeal irritation: nuchal (neck) rigidity, Budzinski and Kernig signs

Seizures

-sudden, abnormal, disorderly discharge of neurons causing sudden and transient alteration in brain function

-imbalance of excitability of neurons (excess glutamate) and the body’s ability for inhibition (GABA)

• impaired inhibition or excessive excitation

-Types

• focal/partial

  • isolated to area without spreading to other areas of brain

  • with or without awareness of themselves

  • some have motor symptoms (tremors, shaking)

• generalized

  • quickly spreads to both sides of brain

  • no awareness of having seizures ‘unconcious’

  • sometimes has motor symptoms

• unknown

-manifestations

• motor symptoms ‘absent seizures’

  • clonic- convulsions

  • atonic- loss of muscle (falcidity, relaxed)

  • tonic- stiff and flexed (nonmoving, hyperextended)

  • myoclonus- short muscle twitches (small tremors)

• non-motor symptoms

  • staring

  • lack of or slight movement

Seizure Stages

-aura stage

• trigger/indication this is happening

• may be excitation of neurons starting

-ictal stage- active seizure portion

• can be tonic, clonic, or absent

-postictal stage

• normally exhausted

• difficult to arouse, nauseated

-longer seizures last the more long term effects it will have on a patient

Epilepsy

-chronic disorder characterized by recurrent seizures

-etiology

• often unknown (50%)

• trauma (children)

• stroke (older adults)

• injury decreases seizure threshold and therefore easier for them to have a seizure

-Status Epilepticus

• prolonged seizure activity of either a seizure longer than 5 minutes or more than 1 seizure in 5 minutes

• risk for major brain damage and death

• refractory SE- seizures lasting longer than 60 minutes

Headaches

-when any pain-sensitive structures in head and neck are stimulated

• meninges, nerves, muscles may get irritated from dilation of blod vessels

-primary- happens in and of itself without other disease process

• common

• chronic or recurrent

• tension- muscle tightness/overuse of neck irritating cranial nerves

• migraines- related to triggers (nausea, vomiting, photophobia, pain on one side, severe throbbing)

• trigeminal autonomic cephalgia (TAC)- vascular dilation irritating nerve

-secondary- caused by another primary condition

• acute

• serious head injury

• infection

• brain tumor- dull, constant, progressive

• sinus- infection/inflammation

• trigeminal neuralgia- irritable trigeminal nerve all of the time triggered by contact with face

Migraines

-theorhetical pathophysiology

• neuronal hyperexcitability → brain triggers → trigeminal nerve irritation → meningeal vessel dilation → pain

-Stages

• prodrome- cravings, fatigue, fluid retention, irritability

• aura- changes in vision and speech, confusion, numbness

• headache- severe pain, nausea, vomitting, poor concentration, photophobia, phonophobia, disability

• postdrome- fatigue, poor concentration, discomfort

Parkinson’s Disease

-neurodegenerative disorder with progressive loss of dopamine-producing cells

• most often cause is unknown

-risk factors

• age- as age increases, higher likelihood of process

• male sex

• family history

• exposure to toxins

• history of head trauma

-pathophysiology

• impairment of dopamine

• substantia nigra (helps initiate movements and fine-tune them) → does not work correctly

• abnormal Lewy bodies (proteins) develop on neurons

-manifestations- Parkinson’s Triad

• bradykinesia (slow movement)- patients want to move but don’t have dopamine to do so quickly

• resting tremors- don’t have dopamine to stop fine motor movement

• muscle rigidity

Amyotrophic Lateral Sclerosis (ALS)

-progressive loss of upper and lower motor neurons

-motor neuron destruction (rapid and progressive) → damaged neurons mean muscles cannot be contracted/used → muscle atrophy → creates paralysis in affected muscles

• does not affect awareness of sensation

-risk factors

• heavy metal toxins

• exposure: cigarettes, environment, occupational

• repeated physical trauma

• heavy physical activity

-manifestations

• ultimately affects all movement and activity

• includes movement of the diaphragm and muscles

• some rapid and some slower progression

• sensation and cognition remain intact

Multiple Sclerosis

-autoimmune demyelination (sensory and motor)

-pathophysiology

• T-cells activated and wrongly attack myelin sheath → inflammation reaction → T-cells activated restarting cycle

• often have flair-ups that create scarring and worse baseline with each one

-manifestations

• slow and gradual onset

• numbness/tingling

• impaired vision and balance (ataxia)

• fatigue

• cognitive and mood changes

• 90% cycles of remission and exacerbation and 10% primary progressive MS

Huntington’s Disease

-genetic disorder with progressive degeneration of basal ganglia and cortex

• mutated chromosome → abnormal DNA replication → synthesis of mutated proteins → deposits in cytoplasm causing cellular degeneration and neurological damage

-manifestations

• motor symptoms

  • hyperkinesia, chorea, athetosis (excessive motion) →

  • hypokinesia, bradykinesia, dystonia (slowed motion and constant muscle contraction)

• emotional and behavioral

  • major depression, mania, irritability, agitation

• cognitive

  • slowed processing

  • impaired judgement

Guillain-Barre Syndrome

-acute peripheral neuropathy of progressive limb weakenss over several days to 4 weeks

-pathophysiology

• typically triggered by viral infection → confusion of immune cells → mistakenly attack body of antigen and myelin sheaths of patients → progressive impaired signal conduction with sensory and motor neurons

• as infection starts to fade, process will reverse

-risk factors

• recent infections

  • campylobacter Jejuni, mycoplasma pneumonia

  • CMV, EBV

• Vaccination (rare) can trigger it

-Manifestations

• starts intoes and progresses up the body

• acute inflammatory demyelinating polyneuropathy

• parashtesia in hands and feet

• symmetrical muscle weakness (starts in legs and ascends)

• severe respiratory muscle weakness

Myasthenia Gravis

-autoimmune disorder creating loss of functioning acetylcholine receptors in the neuromuscular junction

• lose ability to initiate and maintain movement (progressive weakness)

-manifestations

• ocular form

  • droopy eyelids (ptosis)

  • blurry or double vision

• general forms

  • muscle weakness

  • fatigue

  • droopy eyelids

  • blury or double vision

  • limited facial expressions

  • trouble walking

  • difficulty speaking, swallowing, chewing