PATHO EXAM 3: neurologic

Central nervous system

• ____: sensory relay center of the brain; receives all sensory input and sends signals to cerebral cortex for interpretation 

• Limbic system: 4 parts = thalamus, hypothalamus, amygdala, hippocampus

  • Hypothalamus: regulates emperature + ABGs + hormones + hunger

  • Amygdala: emotional, pleasure, sexual behavior  

  • Hippocampus: memories 

• Diencephalon: thalamus, hypothalamus, pineal gland

  • Pineal gland: produce melatonin + control circadian rhythm 

• Reticular activating system (RAS): keeps the cerebral cortex aroused + alert

  • Decrease RAS function = decreased CNS arousal + alertness

• Tentorium cerebelli is the membrane separating brainstem from cerebral hemisphere 

  • Supratentorial = means it relates to smth in the cerebral hemisphere

  • Infratentorial = means it relates to smth in the brainstem, cerebellum, or spinal cord

Coma

Caused by:

• Pathologies of the brain’s supratentorial, subdural, intracerebral + bilateral hemisphere damage 

• Brain stem lesions or metabolic issues that damage the RAS (reticular articulation system)

  • Metabolic issues: severe hypoglycemia, severe hypoxia, neural exctibality (anesthesia, drug addiction, epilpsy/seizures)

Manifestations 

• altered LOC !!!!!

• Breathing patterns 

• Pupil size and reactivity 

• Oculomotor response 

• Motor response 

Different LOC changes

from mild → worst*

• ____: slow and unclear thinking, impaired decision making 

• ____: patient cant determine time, place, person

• ____: decreased movement or speech 

• ____: decreased arousal, falls asleep without stimulation 

• ____: un-arousable EXCEPT by vigorous stimulation → patient withdrawals from painful stimuli

  • Ex: sternal rub or shaking → patient withdrawals ***think: “are you stupid?? (slaps)***

• ____: no movement REGARDLESS of stimuli 

• confusion

• disoriented

• lethargy

• obtunded

• stupor

• coma

Different breathing patterns 

from mild → worst. As we go down this list, the pathology is more significant coma indicator

• ____: hyperventilates first → then apnea

  • person only responds to CO2 bc cerebral cortex is damaged

  • ABG: uncompensated resp alkalosis

• ____: “cresendo-decrescendo” pattern where it’s hyperpnea → then apnea 

  • Bc cerebral cortex is damaged 

  • Commonly seen in congestive heart failure 

  • ABG: no changes tbh 

• ____: constant rapid deep breathing

  • Bc upper pons is damaged

  • Goes on for weeks, months, etc…. So think of it like COPD

  • ABG: Resp alkalosis compensated (bc it goes on for so long, kidneys have time to compensate)

• ____: prolonged “cramp” during inhale + brief exhale

  • Bc middle pons is damaged 

• ____: irregular pause between breaths

  • Bc lower pons is damaged 

• ____: completely irregular breathing; unpredictable rythym

  • Bc medulla is damaged

• ____: deep, slow deep breathing OR deep, slow gasps

  • “End of life” breathing

• post-hyperventilation apnea

• cheyne stokes

• central neurogenic hyperventilation

• Apneusis

• Cluster breathing

• ataxic breathing

• agonal gasping

Pupil size and reactivity (oculomotor responses)

Oculo-vestibular caloric test: water-filled syringe is released into one ear

• Normal result: conjugate (both eyes move to look at the stimulus)

• Abnormal result: disconjugate (one eye doesnt move together to look at the stimulus) OR absent (no movement)

• These results indicate damage to which brain area?

Oculocephalic test (aka doll eyes test): nurse holds eyelid open and asks pt to turn their head to each side 

• Normal result: conjugate (symmetrical eye movement) 

• Abnormal result: disconjugate (asymmetrical eye movement) OR absent 

• These results indicate damage to which brain area?

• brain stem (bc rmb brain stem damage = CN 3 damage)

• brain stem (bc rmb brain stem damage = CN 3 damage)

Different pupil interpretations 

Normal pupils: Small, reactive, regular 

Abnormal pupils:

• Diencephalon issue → constricted and reactive 

• Pons issue → pinpoint

• Midbrain issue → dilated and fixed 

• Compressed 3rd cranial nerve → both eyes fixed; one is dilated + one is normal

Posture responses to brain injury

• Decorticate posture: due to ___ damage 

  • Arms adducted and “stuck” to their chest with flexed wrist

• Decerbrerate posture: due to ____ damage

  • Arms abducted and stuck to patient’s sides with flexed wrist

• cerebral cortex

• midbrain

Alterations in awareness: Delerium

• ACUTE brain dysfunction

• Develops over how many days?

  • often in post-op, ICU, from drug withdrawal, or end of life

• Altered neurotransmitter levels allow inflammatory cytokines to alter BBB → easier for toxins to cross into brain

Delirium types:

1. Hyperactive (aka agitated delirium)

2. Hypoactive

3. Mixed

Manifestations

**note: manifestations fluctuate, so one moment they’re normal but the next moment the have symptoms 

For hyperactive delerium: 

• Autonomic nervous system is overstimulated = aggression, tachypnea, tachycardia, increased body temp, superhuman strength

• Decreased concentration

• Insomnia, restless

• Delusions, hallucinations

For hypoactive delirium 

• Autonomic nervous system ISNT activated

• More subtle, patient is quiet and withdrawals from people

• 2-3 days

____: slow, progressive, irreversible failure of cerebral function NOT CAUSED BY impaired cerebral functions = so cerebral cortex remainds untouched

Caused by: 

• brain inflammation OR abnormal protein accumulation in brain → neurodegeneration and cerebral shrinking → impaired synapse firing → trauma 

Manifestations 

• Memory loss

• Decline in mental ability

• dementia

Alterations of awareness: Alzheimers

• Aka “_____” bc it affects cerebral cortex → memory loss

2 types

• Early alzheimers (aka familial alzheimers): primarily from genetics

• Late alzheimers (aka sporadic alzheimers)

Risk factors for late onset Alzheimers 

• Age 65+

• ApoE gene

• Menopause

• Hypertension, hyperlipidemia, atherosclerosis

• Diabetes or obesity

• Traumatic brain injury 

• Infection 

Pathogenesis for LATE onset Alzheimers (steps)

• 2 main hallmarks of Alzheimers are?

• Process: intracellular neurofibrillary tangles > BBB dysfunction, Dysfunctional mitochondria, Oxidative stress, or Neuro-inflammation > Inability to breakdown overproduced amyloid beta proteins plaque > Intracellular neurofibrillary tangles > loss of synaptic plasticity and transmission, cholinergic dysfunction, neuro-degeneration > Alzheimers > Death

• cerebral dementia

• cant breakdown overproduced amyloid beta protein plaques + intracellular neurofibrillary tangles

Cerebral hemodynamics

• CSF comes from and returns to the blood

• Altered intracranial pressure (ICP), cerebral blood flow (CBF), and O2 delivery 

1. Increased ICP = cerebral edema = decreased CBF = decreased O2 delivery 

Treatment goals if pt has increased ICP

• ICP less than _____

• Cerebral perfusion pressure (CPP) greater than _____

  • although, the widely accepted normal CPP range is _____. the treatment goal is slightly higher for wiggle room i guess?

• CPP formula?

Subarachnoid villi

• CSF (produced by ___) circulates within ____ of brain/ spinal cord

• ____ (little protrusions that act as 1-way valves) secretes CSF into ___ (which collects deoxygenated blood + CSF = becomes intermixed) → blood drains into ____ veins → returns to right side of heart → lungs → rest of body → continuously recycled as normal blood

• Thus, CSF reabsorption (from arachnoid villi into venous sinuses) depends on pressure gradient 

• Damaged subarachoid villi (ex: scar tissue thickens the external surfaces of subarachnoid villi) creates resistance to CSF being pushed out = pressure buildup = increased ICP

• 20 mmHg

• 70 mmHg

• 60-100mmHg

• cranial perfusion pressure = MAP - ICP

  • note: this means that how much blood ur heart pumps will influence ICP and CPP !!

• chorioid plexus

• subarachnoid space

• subarachnoid villi

• venous sinuses

• jugular veins

Increased intracranial pressure

Caused by

• Mass, cerebral edema, excess CSF, hemorrhage 

• Remember the skull is a “rigid box”, so any increase inside brain’s subarachnoid space = increased ICP within entire skull = BAD 

2 compensation methods (which eventually backfire):

• first one (happens in early compensation)

• second one (happens in late compensation)

• temporary CSF displacement into spinal subarachnoid space (or it can also drain into venous sinsues to drain into systemic blood circulation) —> yay decreased ICP —> eventually backfires —> external compression of intracranial veins (which impairs drainage = worsened ICP)

• systemic arterial vasoconstriction via autoregulation (intracranial arteries constrict to maintain constant blood perfusion inside brain) —> eventually backfires —> herniation (basically when brain oozes into normally-empty spaces inside cranium)

Clinical manifestations of increased ICP

Stage 1: _____

• Via displaced CSF + systemic arterial vasoconstrxn autoregulation

• ICP level is within normal limits 

Stage 2: brain expansion

• _____

• SX: confusion, drowsy, increased BP, slight pupillary change, slight breathing change  

Stage 3 and leading into stage 4: ____

• SX:

  • Decreased LOC 

  • Ataxia

  • Cheyne-Stokes breathing (alternating crescendo-decrescendo with apnea)

  • Neurogenic hyperventilation (caused by brainstem dysfunction)

  • Agonal gasping

  • Dilated fixed pupils (starts as unilateral → bilateral)

  • Wide pulse pressure (when systolic is increasing but diastolic is decreasing = increased gap between the two values)

    • Ex: at stage 1 the BP is 120/60 → stage 3 the BP is 200/40 

4.Stage 4: terminal  

• At this stage, brain acidosis + no brain perfusion

• SX:

  • Coma 

  • Resp arrest

  • Fixed dilated pupils

  • No movement 

Interventions

• at which stage is intervention preferable (catch it early)?

• at which stage is intervention CRITICAL?

• at which stage is intervention pointless?

• effective compensation

• brain expansion

• brain hypoxia + brain herniation

• 2

• 3

• 4

Herniation 

**Normally, the brain has spaces that are empty (see in diagram) that become distorted/compressed due to herniation 

**rmb: tentorium cerebelli is a membrane that divides cerebrum (above) from cerrbellum (below)

• Supratentorial herniation: occurs ABOVE the tentorium cerebelli 

• Infratentorial herniation: occurs BELOW the tentorium cerebelli

____: Increased fluid within brain tissue itself 

• Results in distorted blood vessels → displaced brain tissue → herniation  

Manifestations

• Decreased LOC

• Increased ICP

Types

• Vasogenic: due to ____ → damaged BBB (causes CSF fluid to leak into ___) → increased ICP → ischemia 

• Cytotoxic (metabolic): due to ____ → ___ failure → parenchymal tissue cells swell

• Interstitial: due to ____ → CSF leaks from ventricles into brain tissue (specifically periventricular white matter )

• cerebral edema

• increased capillary permeability

• extracellular space

• toxins

• cell’s sodium potassium pump failure

• increased pressure inside brain’s ventricles

Alterations in muscle tone 

Hypotonia 

• Patient has passive movement without resistance due to loss of nerve transmission from damage to which motor neuron (upper or lower?)

  • specifically damage to brain’s bulbar area, anterior horn area, or damage to the affected muscle itself

• limp, atrophied extremities; excessive movement when displaced (meaning it flops right down if picked up)

• seen in patients with what conditions?

• Does this have babinski reflex?

• Does this have fasciculations?

• How does this affect DTR?

Hypertonia 

• Patient has resistance to passive movement 

• due to damage to which motor neuron (upper or lower?)

  •  specifically damage to motor cortex, brainstem, spinal cord

• seen in patients with what conditions?

• Does this have babinski reflex?

• Does this have fasciculations?

• How does this affect DTR?

• LMN

• cerebral palsy, polio, ALS, myasthenia gravis

• No

• Yes

• weak or absent deep tendon reflex

• UMN

• parkinsons, multiple sclerosis, stroke, cancer

• Yes

• No

• hyper-active deep tendon reflex

Decussation of Affernet VS Efferent pathways

• Decussation: crossing over to opposite side of the body

• The CNS is mostly crossed (right side of brain controls left side of body, and vice versa)

• Afferent pathways for pain/temp cross the ___

  • Ex: spinal cord lesion → creates sensory abnormalities 

• Efferent pathways cross the ____

  • Ex: stroke in brain’s left side → right side muscle paralysis 

  • Relates to pyramidal movement bc it carries signals from brain → to muscles

• spinal cord

• cerebellum

Pyramidal Motor Tract

• Pyramidal is responsible for ____ whose transmission crosses @ ____

Manifestations of pyramidal dysfunction:

• Paralysis of voluntary movement (ex: person cant wipe their eye)

• Increased DTR (ex: clonus in DTR)

• Is there babinski reflex?

• Involves ____: when limb stiffness is speed-dependent

  • Ex: moving a patient’s limb slow is not gonna resist VS moving a patient’s limb fast is gonna have more resistance)

Extrapyramidal Motor Tracts

• Extrapyramidal is responsible for _____ whose transmission crosses @ ____

Manifestations of extrapyramidal dysfunction:

• normal voluntary movement (ex: person can wipe eye just fine)

• Normal DTR

• Is there babinski reflex?

• Involves ____: when limb stiffness ISNT speed-dependent 

  • Ex: moving a patient’s limb is gonna be constantly ratchet regardless of speed
    

• precise controlled voluntary movement

• medulla

• Yes babinksi

• spasticity

• smooth coordinated involuntary movement

• basal ganglia

• no babinski

• cogwheel rigidity

_____: Neuro-degenerative disorder that affects both UMN and LMN

• Ex: your house is on fire but you cant run but you can feel yourself burning and choking on smoke

• Progressive muscle weakness → respiratory failure → death 

• 2 types:

  • Familial ← rare (due to gene mutation)

  • Sporadic ← most common (its a random and unknown cause)

Pathogenesis 

• We dont know!

Manifestations

• Flaccid paralysis 

• Muscle wasting, hypotonia, muscle atrophy

• Dysphonia, dyspnea

• Fascicultations

• Sialorrhea (excess drooling)

ALS

____: an extrapyramidal condition due to dopamine and AcH imbalance

Pathophysiology

• Destruction of dopamine cells @ the _____ of basal ganglia → depleted dopamine supply → degeneration of dopamine pathway → imbalance of dopamine and AcH → extrapyramidal dysfunction SX (tremors specifically pill rolling tremor*, rigidity, bradykinesia)

Manifestations 

• Pill rolling tremor

• Rigidity 

• Bradykinesa

• Slow walking + short shuffling steps

• Stooped posture with wide stance

• Masked facial expression (wide eyed staring expression )

• flexed and abducted arms held at their side

• Drooling 

Treatment

• Drug therapy: Levadopa, Amantadine, anticholingerics, antihistamines

• Rehabilitaiton

• Surgery

• Stem cell implant 

• substantia nigra

____: progressive autoimmune inflammatory demyelinating disorder → reduced nerve transmission 

Pathophysiology 

• ____ cells cross BBB → attacks myelin → degeneration of nerve axons → irreversible tissue damage → scarring 

• On and off SX (remyelination and exacerbations)

Clinical manifestations

• Visual impairment (either unilateral or bilateral)

• Cranial nerve deficits (from brainstem lesion)

• Thinking + motor + sensory impairment 

• Depression

• Ataxia, nystagmus

• Spastic partial paralysis 

• Decreased DTR

• Decreased bladder control → incontinence 

• multiple sclerosis

• Tcells and Bcells

____: ACQUIRED inflammatory disease preceded by a viral/or bacterial infxn → causes demyelination of peripheral nerves (arms/legs)

• Humoral and cellular immune reaction 

• On/off SX

• Acute onset is characterized by ________

Manifestations 

• Paresis (muscle weakness), parasthesia, (pins and needles), paralysis

• Dysphagia, choking

• Dysarthria (impaired speech)

• Decreased DTR

• guillan barre syndrome

• ascending motor paralysis (paralysis begins in extremities > spreads to resp system > spreads to face/mouth/throat)

____: chronic autoimmune disease involving anti-AcH antibodies

Pathophysiology

• ____ blocks AcH receptor at neuromuscular junction → decreased nerve transmission → weak muscle contraction → weak muscles, eyes, throat

Manifestations

• Diplopia, ptosis

• Droopy face

• Dysphagia

• Dysarthria (impaired speech), choking

• Drooling 

• Respiratory distress

Diagnosis

• involves what test + what drug + how does this work?

Treatment 

• ?

2 possible complications of anticholinesterase treatment:

1. ____: AcH degradation caused by NOT ENOUGH drug

• occurs how long after adminsitration?

• SX?

• nursing process?

2. ____: anticholinesterase drug toxicity

• occurs how long after adminsitration?

• SX?

• nursing process?

• myasthenia gravis

• IgG

• Tensilon test that uses Edrophonium (acetylcholinesterase inhibitor) which gives patient a temporary boost in muscle strength. after administering Edrophonium, if the patient’s muscle weakness improves = positive for Myasthenia Gravis

• Acetylcholinesterase inhibitor

• Myasthenia crisis

• 4 hrs after treatment is given

• Acute resp failure + severe quadriparesis

• give higher dose or give more frequent dosing thru the day

• Cholinergic crisis

• less than 1 hr after treatment is given

• Acute resp failure + severe quadriparesis + diarrhea and sialorrhea

• decreased dose or give spaced out dosing thru the day

Brain injury (GENERAL CONCEPT)

• Primary injury is from DIRECT impact (ex: skull fracture, laceration, hemorrhage)

• Secondary injury is iNDIRECT and occurs secondary to primary injury (ex: cerebral edema, increased ICP, hypoxia, etc….)

Molecular pathophysiology of brain injury

• Brain trauma → membrane depolarization → opened N/K/Ca channels and released glutamate (excitatory neurotransmitter) →  intracellular edema and Ca overload→ mitochondrial dysfunction → apoptosis + ROS → inflammation and vasogenic edema (BBB leaking) → ischemia + neuron damage →  neurologic deficit 

Cerebral hemorrhage and herniation 

Hematoma (collection of blood) → takes up space and can develop into clot → increased ICP

Hemorrhage (actively bleeding) → spreads and takes up space → increased ICP

• Types: sub-arachnoid, epidural, subdural, intracerebral 

  • Epidural hemmorage is usually ___ bleeding = faster + more blood leaking

    • needs treatment ASAP  

  • Subdural hemmorage is usually ___ bleeding = slower + less blood leaking

    • doesnt need to be treated as fast as epidural bleed, BUT more dangerous bc it goes undetected = higher mortality risk
      

Craniotomy 

• treatment surgery fro hematoma/hemmorhage

• post-op SX will definitely have headache + risk of cerebral edema, bleeding, seizures

• arterial

• venous

____: blood leaks from defective vasculature into sub-arachnoid space

• can be caused by Aneurysm or congenital vessel malformation → inflammatory response 

• High mortality rate within ___ hours

Manifestations

• which SX is the most obvious one?

• other SX are?

• subarachnoid hemmorhage

• 72 hrs

• “"worst headache of my life”. caused by warning micro-bleeds that occur days before actual rupture

• kernig syndrome (painful knee extension)+ brudzinski sign (when forced flexion of stiff neck causes automatic knee flexion) + nuchal rigidity, photophobia

Skull fracture

3 types

____: broken skull with an open scalp wound

____: brain is exposed

____: fractured base of skull → cranial nerve damage + CSF leak 

• CAN get infected and develop into meningitis (inflamed and infected brain/spinal cord)

• Manifestations?
  

• compound skull fracture

• open brain injury

• basilar skull fracture

• racoon eyes (brusing around eyes) + battle sign (bruising behind ear)

Seizures

• Sudden, transient altered brain function caused by abrupt, explosive, disorderly neuron firing

Types

_____: affects brain unilaterally

___: affects brain bilaterally

• describe tonic-clonic?

• breathing stops = aspiration risk from uncontrolled saliva

• person may/may not experience prodroma (warning sign days before seizure) or aura (warning sign right before seizure)

_____: recurrent seizures

Seizures continued 

• During tonic phase, electrical activity spreads to cerebral cortex and brain stem

• During clonic phase, neuron is undergoing hyperpolarizaton (involves back-and-forth switching of neurons firing and not firing = thus the jerking motions) → seizure eventually ends 

• Describe how seizures affect cerebral metabolism —> how it leads to neuron degeneration?

• focal seizure

• generalized seizure (aka grand mal or tonic-clonic seizure)

• tonic comes first (muscle rigid) —> clonic comes after (violent, rythmic jerking muscle contractions)

• epilepsy

• seizures use up hella energy and hella O2 consumption —> depletion of glucose + O2 —> metabolic acidosis + hypoxia —> neuron cell death —> neuron degenration

Tonic clonic seizures (continued_

• Post-seizure state: headache, confusion, tired, nauseous, muscle sore, weak

Complications of seizures:

• ____: the 2nd seizure before recovery from the previous seizure OR a prolonged continuing seizure (potentially last over 30 mins) → can risk cerebral hypoxia

• Aspiration

• Brain damage

• status epilepticus

• cerebral hypoxia

Stroke aka Cerebrovascular accidents (CVA)

Pathophysiology 

• Ischemia → hypoxia → Myocardial infarction → creates zone of hypoxia in brain 

  • if we know where the zone of hypoxia is in the brain, we can re-establish bloodflow in that zone to prevent further damage/or necrosis of brain tissue

Types of strokes

____: fragments that breaks off from thombus formed outside of brain 

• MOST COMMON stroke

• ex: seen in Afib or mechanical heart valves

____: arterial occlusions cause by thrombus formation inside brain’s arteries/veins 

____: caused by intracerebral hemorrhage or subarachnoid hemorrhage

Manifestations of stroke

• Facial drooping

• Dysphasia (speech trouble)

• Swallowing trouble

• Paralysis 

• Agonal breathing 

Treatment 

• Thrombolytic drugs

• Drug contraindications:

  • Antiplatlet drugs (ex: Aspirin)

  • if INR is above 1.7 seconds

  • if PT is above 15 seconds

  • Platelet count below 100,000

• ischemic embolic stroke

• ischemic thrombotic stroke

• hemorrhagic stroke

Cerebral infarction

• Cerebral “zone of hypoxia” → can develop into ischemia (if not treated ASAP)

• If we know where the zone of hypoxia is in the brain, we can re-establish bloodflow in that zone to prevent further damage/or necrosis of brain tissue

• Hemorrhaging can occur in the zone of hypoxia → increased pressure from the extra blood compresses brain tissue → ischemia, edema, increased ICP, → necrosis