NEURO (TBI-Stroke-HA-Neurodegenerative) Flashcards
In TBI, approx how many deaths per year occur
52,000
Leading cause of death & disability in children/adults from 1-44 y/o
Traumatic brain injury
Who are more likely to experience TBI?
Males, twice as likely than females
Non-degenerative, non-congenital insult to brain from external mechanical force
TBI
Associated diminished or altered state of consciousness
TBI
TBI is possibly leading to permanent or temporary impairment of ______, _______, & ________ functions (CPP)
Cognitive, physical, & psychosocial
What are the types of TBI
- closed brain injury
- open brain injury
A type of TBI, without the skull being broken or penetrated & the brain not being exposed
Closed brain injury
Type of TBI: When the rapid movement of the head backward and forward (acceleration-deceleration movement) causes the brain to move inside the skull & slam against its hard inner bone.
Closed brain injury
What are the two closed head injury
- Coup injury
- Countercoup injury
Sudden hyperextension of the head & neck forces the brain forward against the front of the skull
Coup injury
Hyperflexion of the head & neck forces the brain backward against the skull
Countercoup injury
Combination of coup & countercoup injury
Whiplash
C1 & C2 damage (use of neckbrace)
Paraplegia
N/V
Dizziness
Headache,
V diplopia (severe),
H diplopia (mild)
Transient visual loss (Amaurosis fugax)
Concussion
Process where u can obtain bruise/blood clot
Contussion
If the contusion hasn’t caused infarction, how can we can stop temporary amnesia from becoming permanent?
- Warm compress: dilate BV to let blood flow
- Cold compress: ease throbbing/symptom
If there’s external force, don’t let px sleep for 3hrs to prevent infarction even w/o wc
Which part of the brain is affected with temporary/selective amnesia?
Any part of the brain
Which part of the brains affected in permanent amnesia?
Hippocampus
Open or penetrating head injury
Open brain injury
In Open brain injury, TBI can be ______ or _______, damage may be isolated to one specific area of brain in focal injuries or widespread in case of diffuse injuries
Focal or diffuse
Etiology of Open brain injury (FVVS)
- Falls
- Vehicle-related collisions
- Violence (gunshot wounds, child abuse, shaken baby syndrome)
- Sports injuries (soccer, boxing, football, extreme sports)
TBI is divided into
- Primary injury / brain damage
- Secondary injury / brain damage
Induced by mechanical force & occurs at the moment of injury
Primary injury
Not mechanically induced, may be delayed from moment of impact & may superimpose injury on a brain already affected by mechanical injury
Secondary injury
Cause subdural hemorrhage, drown the brainstem & lead to loss of voluntary response
Secondary injury
Secondary injury cause __________, drown the brainstem & lead to loss of voluntary response
Subdural hemorrhage
What part of brain is affected if there is a problem in posture/walking
Cerebellum (drowning)
What are the two main mechanisms of Primary brain damage
- Contact
- Acceleration-deceleration
Mechanism of primary brain damage which result in fracture to the skull & surface contusions
Contact
Mechanism of primary brain damage which results in unrestricted movement of the head & leads to shear, tensile, & comprehensive strains
Acceleration-deceleration
Primary brain damage: These forces can cause _________,__________,________
Intracranial hematoma, diffuse vascular injury, & injury to cranial nerves & pituitary stalk
The most common cause of death & clinical deterioration after TBI
Intracranial Hematoma
What are the three categories of hematomas (ESS)
- Epidural hematomas
- Subdural hematomas
- Subarachnoid hematomas
Hematoma: caused by fracture of temporal bone & rupture of middle meningeal artery
Epidural hematoma
Hematoma: such hematomas are usually caused by rupture of the bridging veins in the subdural space
Subdural hematomas
Hematoma: these result from damage to blood vessels in the posterior fossa stalk
Subarachnoid hematomas
Extracranial hematoma (SIN)
- Scalp lacerations
- Nasal injuries
- Injuries to face & neck can lead to significant blood loss
Occurs hours, days after traumatic event.
Injury may result from impairment in cerebral blood flow after TBI
Secondary brain damage
Decrease in cerebral blood flow (CBF) are results of _______,________, or __________
Local edema, hemorrhage, or increased intracranial pressure (ICP)
As a result of inadequate perfusion, cellular ion pumps may fail, causing a cascade involving intracellular calcium & sodium
Secondary brain damage
____________ may contribute to cellular destruction
Resultant calcium & sodium overload
Excessive release of excitatory amino acids, such as ________&________ exacerbates failure of ion pumps
Glutamate & aspartate
As the cascade continues, cells die causing ______,______&__________
Free radical formation, proteolysis, & lipid peroxidation
In secondary brain damage all the factors ultimately cause
Neuronal death
Extracranial causes of SBD (FF)
-failure of adequate cerebral perfusion from circulatory shock
-failure of cerebral oxygenation from disturbance of pulmonary ventilation from: (aspiration, instability of chest wall (flail chest), neurogenic disturbances of ventilatory drive)
Intracranial causes of SBD (RC)
-rise in ICP due to mass lesions & cerebral edema leading to fall in cerebral perfusion pressure & to herniation of brain is a major factor in poor outcome
-cerebral autoregulation impraired
Signs & symptoms of Mild TBI (LMH-DND)
- loss of consciousness for a few seconds
- memory/concentration problems
- headache
- dizziness/loss of balance
- N/V
- difficulty sleeping
Signs & symptoms of moderate to severe TBI (LIPS-LW)
- loss of consciousness several mins to hours
- slurred speech
- inability to awaken from sleep
- weakness in fingers & toes
- loss of coordination
- persistent headache/ headache that worsens
Children symptoms of TBI (CCCPS)
- change in eating/nursing habits
- persistent crying & inability to be consoled
- change in ability to pay attention
- change in sleeping habits
- sad/depressed mood
Presentation: Cognitive problems (JAMS-LPD)
-Memory
-Learning
-Problem solving
-Speed of mental processing
-Judgement
-Attention or concentration
-Decision making
Presentation: Physical changes (SSCC-PL)
-Spasticity
-Physical paralysis
-Chronic pain
-Sensory
-Loss of stamina
-Control of bowel & blader
5th leading cause of death in US, one person dying every 4 mins
Stroke
Second leading cause of death in the world
Stroke
Approx ________ people have a stroke each year, one every 40 secs
800,000
Occur due to problems with blood supply to the brain; either the blood supply is blocked or a blood vessel within the brain ruptures, causing brain tissue to die
Stroke
Clinical syndrome of rapid onset of cerebral deficit lasting more than 24hrs or leading to death with no apparent cause other than a vascular one
Stroke
Rapid loss of brain function due to disturbance in the blood supply the brain
Stroke
A stroke happens when blood flow to a part of the brain stops and is sometimes called
Brain attack
Most common cause of severe physical disability
Stoke
Prevalence of stroke in India:
Death rate:
PrevalenceL 1.54 per 1000
Death rate: 0.6 per 1000
Types of stroke (HIT)
-Ischemic stroke
-Hemorrhagic stroke
-Transient Ischemic Attack (TIA)
Most common form of stroke, 85% of strokes
Ischemic stroke
Type of stroke caused by blockage or narrowing of arteries that provide blood to the brain resulting in severely reduced blood flow
Ischemic stroke
Ischemic stroke: blockages are often caused by _________
blood clots
Clots can be caused by fatty deposits within the arteries called
Plaque
Type of stroke: Caused by arteries in the brain either leaking or bursting open
Hemorrhagic stroke
Hemorrhagic stroke: ruptures can be caused by conditions such as (BATH)
-Hypertension
-Trauma
-Blood thinning medications
-Aneurysms (weakness in blood vessel walls)
What are the two types of hemorrhagic stroke
-Intracerebral hemorrhage
-Subarachnoid hemorrhage
Most common type of hemorrhagic stroke, occurs when brain tissue is flooded with blood after an artery in the brain bursts
Intra cerebral hemorrhage
Second type of hemorrhagic stroek, less common, bleeding occurs in subarachnoid space - area between brain & the thin tissues that cover it
Subarachnoid hemorhage
flow of blood to the brain is only briefly interrupted
Transient Ischemic Attack (TIA)
How is TIA similar to Ischemic stroke
they are often caused by blood clots or other debris
should be regarded as medical emergencies
TIA
referred to as “mini strokes”, lasts below 24 hours
TIA
serve as warning signs for future strokes & indicate that there is partially blocked artery or clot source in the heart
TIA
Between ______% will have major stroke within 3 months of TIA
10-15%
due to vasoconstriction induced by stress
TIA
Causes of TIA (LUCS)
- Large artery atherosclerosis
- Cardio-aortic embolism
- Small artery occlusion
- Undetermined cases:
unknown - cryptogenic embolism
unknown - other cryptogenic
unknown - incomplete evaluation
Signs of TIA (WTV-HD)
- Weakness (sudden loss of strength/numbness in face, arm, leg)
- Trouble speaking (sudden difficulty speaking/understanding, confusion)
- Vision problems (sudden trouble w vision (amaurosis fugax)
- Headache (sudden severe & unusual headache)
- Dizziness (sudden loss of balance, w any of the above signs)
Symptoms of TIA (CHNTT)
- Confusion (incl; trouble speaking & understanding)
- Headache (w altered consciousness or vomiting)
- Numbness of face, arm/leg on one side of body
- Trouble seeing in one or both eyes
- Trouble walking, including dizziness & lack of coordination
Diagnosis of stroke
F.A.S.T. - way to remember signs of stroke can help identify onset of stroke quickly
What does F.A.S.T. stand for
Face drooping: tries to smile & one side of face droop
Arm weakness: tries to raise both arms, one drifts down
Speech difficulty: tries to repeat a phrase & speech is slurred
Time to call 911: if any are observed, contact emergency
Diagnostic tests of stroke
- Physical exam
- Blood test
- CT scan
- MRI scan
- Carotid ultrasound
- Cerebral angiogram
- Echocardiogram
Treatment for stroke
Ischemic: Aspirin (given as injection), Carotid endarterectomy, Angioplasty
Hemorrhagic: Drugs that reduce pressure in the brain, Surgery to repair problems w blood vessel & remove small AVMs if not too big or deep in the brain
Rehab for stroke
- Speech therapy
- Physical therapy
- Occupational therapy
- Joining support group
- Support from friends & family
Prevention of stoke
- Eat healthy diet
- Maintain healthy weight
- Exercise regularly
- not smoking
- avoiding alcohol/moderate consumption
What causes vision deficits after stroke?
- damage caused to specific regions of visual cortex or its connecting neural network
- loss of vision is due to damage done to part of brain that processes visual info transmitted to it using eyes as conduits
about ______ nearly 1 of 4 in people had previous stroke
185,000
about ____% of all strokes are Ischemic strokes
87%
______% of people hospitalized w stroke are younger than 65
34%
____% of people suffer from stroke experience changes in their vision. _____% experience permanent visual deficit
66%, 20%
Types of Post-Stroke Vision Deficits
- Hemianopia
- Quadrantanopia
- Scotoma
- Tunnel vision
Type of post-stroke vision deficit: blindness in one half of VF
Hemianopia
Type of post-stroke vision deficit: loss of vision occur in quarter of VF
Quadrantanopia
Type of post-stroke vision deficit: spotty vision/small area of blindness than hemi/quadrantanopia
Scotoma
Type of post-stroke vision deficit: loss of peripheral vision that mimics looking thru a tunnel
Tunnel vision
3 recovery options of stroke vision deficits
- Vision restoration (Neuroplasticity, Vision restoration therapy)
- Vision compensation (Neuroeyecoach)
- Substitution (use of optical aids)
study of how nervous system develops, its structure, what it does
Neuroscience (Neural Science)
specialized cell, transmit commands from the brain to control organs & muscles, thought, feeling & movement
Neurons
controlling unit of body, comprises billions of cells (neurons) which form communication center (nervous system)
Brain
progressive loss of nerve structures & function, leads to loss of cognitive abilities
Neurodegeneration
_______ building blocks of nervous system, doesnt reproduce themselves when damaged
Neurons
key aspect of large number of diseases that come under umbrella of “neurodegenerative diseases”
Neurodegeneration
most notable degenerative diseases
Alzheimer’s, Parkinson’s, & Huntington disease
progressive ND that mostly affects px in later stage of life
Alzheimer’s disease
typical symptoms are loss of cognitive function, including emotion, learning & memory processing skills leading to dementia
Alzheimer’s
_____% of the risk is believed to be genetic w many genes involved. And what ND?
70%, Alzheimer’s
Risk factors of Alzheimer’s (HDH)
- history of head injuries
- depression
- hypertension
pathological impression of Alzheimer’s is characterized by deposition of _________ in the brain parenchyma & accumulation of ________ within neurons
amyloid-beta (AB) protein plaques, tau proteins
Typical symptoms of Alzheimer’s
Loss of cognitive functions including:
- emotions
- learning
- memory processing leading to dementia
These protein plaques interfere with synaptic transmission & neuron-neuron communication leading to _________
Neuronal death
_____________ within neurons form tangles & block transportation of nutrients or jam other vital cellular factors throughout the cell which becomes the reason for _______ in Alzheimer’s
Tau proteins, cell death
Symptoms of Alzheimer’s (3P-3D-2M-F)
- Memory loss/changes in memory
- Difficulty performing familiar tasks/routine chores
- Drastic changes in personality
- Misplacing things in inappropriate places
- Problems w abstract thinking
- Forgetting words or substituting inappropriate words
- Problems speaking, writing, reading, understanding
- Disorientation to time & place
- Poor/decreased judgement
typically considered chronic, progressive neurodegenerative movement disorder
Parkinson’s disease
causes death of the vital nerve cells in the area of brain called substantia nigra
Parkinson’s
Parkinson’s causes death of the vital nerve cells in the area of brain called ________
substantia nigra
as Parkinson’s progresses, amount of dopamine produced from brain ______, leading to person unable to control movement normally
decreases
in Parkinson’s, dying neurons produce _________ which acts as a messenger & sends messages to part of the brain that controls movement & coordination
Dopamine
Parkinson’s: proteosomal & lysosomal system dysfunction & reduction in mitochondrial activity due to __________ also cause cell death
genetic mutation
Parkinson’s: activated neurons over expressing proteins lead to early activation of microglia & release of various inflammatory mediators such as:
IL-1, IL-6, TNF-α
Parkinson’s: reactive __________ & _______ enhance oxidative stress & trigger cell-death pathways
oxygen/nitric oxide species & prostaglandins
Symptoms of Parkinson’s
- Depression, sleep disorders, weight loss
- Forced closure of eyelids (blepharospasm)
- Orthostatic hypotension
- Constipation, micturition disorders, sexual problems
- Difficulty speaking/swallowing, excessive salivation, respiratory problems
- Increased sweating
- Bowing of shoulders, swelling of feet
chronic neuroinflammatory, progressive, degenerative disorder of CNS characterized by demyelination of nerve fibers of brain & spinal cord affecting people between 20-40
Multiple sclerosis
initially triggered by a virus genetically susceptible individuals
Multiple sclerosis
subsequent antigen-antibody reaction leads to demyelination of axons i.e; autoimmunity
Multiple sclerosis
Symptoms of Multiple Sclerosis
- Fatigue
- Depression
- Memory change
- Pain
- Spasticity
- Tremor
- Double vision/Vision loss
- Weakness
- Dizziness/Unsteadiness
- Numbness/Tingling
- Ataxia
- Speech disturbance
- Bladder/Bowel/Sexual dysfunction
rapidly progressive neurodegenerative disease that leads to dementia
Huntington’s disease
typically presents w alterations in mood & change in character, defects in memory & attention
Huntington’s
progresses to a movement disorder consisting of involuntary & rapid motions
Huntington’s
usually not recognized until px is in their early 30’s
Huntington’s
there is a ______% chance that a child whose parent has Huntington’s will have the disease
50%
Huntington’s: caused by an autosomal dominant mutation on either of an individual’s two copies of a gene called
Huntingtin
faulty gene that causes Huntington’s is found on
chromosome number four
The normal copy of gene produces protein called “Huntingtin” but faulty gene contains abnormal region called
CAG repeats
Huntington’s: expanded polyglutamine region of pathological form of protein causes impairment of the ubiquitin-proteasome system (True/False)
True
Huntington’s: dysfunctional protein is removed & destroyed as it should be (True/False)
False: dysfunctional proteins is NOT removed & destroyed as it should be
Huntington’s: cells in brain, specifically basal ganglia & parts of cortex are NOT sensitive to effects of abnormal huntingtin. This makes them function WELL & NOT DIE (True/False)
False: cells in brain, specifically basal ganglia & parts of cortex are VERY sensitive to effects of abnormal huntingtin. This makes them function POORLY & eventually die
Symptoms of Huntington’s (Movement)
Movement:
- Choreic movements
- Twitching
- Balance problems
- Tracking problems
- Rigidity & dystonia
Symptoms of Huntington’s (Cognitive)
Cognitive:
- As HD progresses, ability to concentrate becomes more difficult
- Difficulty driving, keeping track of things, making decisions, answering questions, lose ability to recognize familiar objects
- Over time, judgement, memory, & other cognitive functions begin to deteriorate into dementia
Symptoms of Huntington’s (Psychiatric)
- Early symptoms: subtle, varied & easily overlooked/misinterpreted
- Depression - most common symptom & develops early in course of disease
Signs of depression: - Hostility/irritability
- Inability to take pleasure in life (anhedonia)
- Lack of energy
- Hallucinations
major hallmark of neurodegenerative disease
abnormal deposition of aggregates of misfolded proteins (proteinopathies) that lead to cell dysfunction & eventually cell death
pain/discomfort in head, scalp, or neck
Headache
one of the most common of all human physical complaints
Headache
HA: a stress response, ________(migraine), _________(tension headache), or combination of factors
vasodilation, skeletal muscle tension
up to _____% of adults have severe HA each year
25%
up to ____% have daily/near-daily HA
4%
Lifetime prevalence of HA
90% or more
Types/classification of HA
- Primary headache
- Secondary headache
Type of HA: not caused by underlying disease, trauma, or medical condition
Primary HA
accounts 90% of all headaches
Primary HA
most px presenting with HA have ___________
Primary HA syndromes
Primary HA: more common
Episodic headache
Primary HA: attacks occurring more frequently than 15 days/month for more than 6 months
Chronic headache
<2% of headaches in primary care offices
Secondary headache
caused by exogenous disorders
Secondary HA
What are the exogenous disorders caused by secondary HA: (MISH-VN)
- Head trauma
- Vascular disease
- Neoplasms
- Substance abuse/withdrawal
- Infection/inflammation (meningitis)
- Metabolic disorders (hyper/hypogyclemia)
What are the Primary Headache Syndromes
- Tension type HA
- Migraine
- Trigeminal Neuralgia
- Cluster HA
Primary HA type: most common (69%), episodic or chronic
Tension HA
Primary HA type: primary disorder if CNS pain modulation
Tension HA
Precipitating factors of Tension HA (SUICEDS)
- Stress
- Sleep deprivation
- Uncomfortable stressful position/bad posture
- Irregular meal time (hunger)
- Eyestrain
- Caffeine withdrawal
- Dehydration
Tension HA signs & symptoms (BLGN)
- Gradual, onset, radiate forward from occiput
- Bilateral, dull, tight, band-like pain
- Less in morning, pain increase as day goes on
- No accompanying NV, throbbing, sensitivity to light, sound, or movement
Management of Tension HA
- Paracetamol, Aspirin, NSAIDs
- Behavioral approach-relaxation
- Chronic-amitriptyline
Primary HA type: 2nd most common (16%)
women (15%), men (6%)
Migraine
Primary HA type: severe, episodic, unilateral, throbbing pain
-NV, sensitivity to light, sound, movement
-genetic predisposition
Migraine
What are the three theories of Migraine?
- Vascular theory
- Second theory
- Biochemical changes
Migraine theory: vasoconstriction followed by vasodilation resulting in changes in blood flow causing throbbing pain
Vascular theory
Migraine theory: pain results from muscular tension
Second theory
Migraine theory: changes in serotonin levels
Biochemical changes
Migraine triggers (3S-2F-CH)
- Flashing lights, loud sounds, strong odors
- Stress
- Hunger
- Fatigue
- Smoking
- Menstruation, pregnancy, menopause, oral contraceptives
- Sleep changes
- Caffeine, chocolate, tyramine
Classical Migraine or Migraine with AURA symptom triad: (PAN)
- Paroxysmal headache
- Nausea &/ Vomiting
- Aura of focal neurological events (visual) 20-25%
Medical term for aura
Scintillating scotoma
flashing lights, silvery zigzag lines moving across the VF over a period of 20 mins
Aura
sometimes leaving trail of temporary VF loss
Aura
spreading front of tingling & numbness from one body part to another
Sensory aura
Common migraine or Migraine without AURA
- Paroxysmal headache
- Vomiting +/-
- NO AURA
Diagnosis of Migraine must at least have 2 of the ff (MUTA)
- Unilateral pain
- Throbbing pain
- Aggravation by movement
- Moderate/severe intensity
Diagnosis of Migraine must at least have 2 + at least 1 of the ff:
-Nausea/Vomiting
-Photophobia & phonophobia
Management of Migraine: Non-drug treatment
- Avoid Ha triggers: foods, drugs, activities
- Avoid frequent abortive treatment
- Stop smoking
- Normalize sleeping & eating
- Exercise
- Relaxation & biofeedback
- Psychotherapy
Preventive treatment of Migraine
- Tricyclic antidepressants (first-line) - Amitriptyline
- Beta-blockers (first-line) - Atenolol, Nadolol
- Ca++ channel blockers (less effective) - Verapamil- most commonly used
- Anticonvulsants (2nd line) - Valproate & Topiramate - quite effective
- Gabapentin
- Lamotrigine, Levetiracetam
- Pregabalin
- Ergots: rarely used, side effects problematic. Methysergide: fibrosis (use 6 months max)
- MAOIs: can be very effective. Tyramine - free diet a must, Numerous drug interactions
Abortive Therapy for Migraine
- Simple & combined analgesics (NSAIDs)
- Mixed analgesics (Barbiturate + simple analgesics)
- Ergot derivatives
- Triptans
- Opioids
Migraine: Triptans
- Serotonin 5-HT1 agonists
- Reduce neurogenic inflammation
- Most effective if used at onset of HA or aura, though maybe helpful at other phases
- Used specifically for Migraines
- For nonresponders, try ergots (act on NE, DA, other receptors)
Migraine: Drugs to avoid
- Butorphanol nasal spray
- Meperidine
- Overuse of any short-acting analgesic (opioid, triptans)
lancinating pain in 2nd & 3rd divisions of trigeminal nerve, >50 yrs
Trigeminal Neuralgia
severe, brief, repetitive pain causing px to flinch
Trigeminal Neuralgia
Trigeminal Neuralgia: touching trigger zones
Washing
Shaving
Eating
Cold wind
compression of trigeminal N by aberrant loop of cerebellar arteries as nerve enters brainstem
Trigeminal Neuralgia
occurs due to plaque of demyelination in trigeminal root entry zone
Multiple sclerosis
caused by other benign compressive lesions
Trigeminal Neuralgia
Management of Trigeminal Neuralgia
- Carbamazepine
- Intolerant-Gabapentin/Pregabalin
- Injection of alcohol into peripheral branch of nerve
- Posterior craniotomy to relieve vascular compression of trigeminal nerve
HA occur during a short time span
Cluster headache
The cluster then recurs ______
periodically
A typical cluster HA may last _____ weeks with _____headaches/day during the cluster
4-8weeks, 1-2 headaches/day
Cluster HA male to female ratio
5:1
Signs & symptoms of Cluster HA
- abrupt onset of HA originating in eye & spreading over the temporal area
- pain extremely severe & last 20-60 mins
- The HA associated w:
Nasal stuffiness
Rhinorrhoea
Redness of the eye
Flush & edema of the cheek
Management of cluster HA (Acute)
- Oxygen inhalation 100%
- Triptans/ergots
- Indomethacin
Management of cluster HA (Chronic/Preventive)
- Verapamil, lithium
- Valproate, topiramate
- Prednisone burst
- Melatonin
- Ergots
persistent, recurring headache in the setting of regular analgesic use, continues until medication is stopped
Medication Overuse Headache
often responsible for “transformation” of episodic into chronic HA
Medication Overuse Headache
band-like pressure
Tension-type Headache
half head throbbing
Migraine
periorbital sharp
Cluster headache
Cluster HA vs Eyestrain
Cluster (non-ocular) - relieved by meds, pain scale is >7, associated w sinusitis
Eyestrain (asthenopia) - relieved with rest, pain scale: 5
