Cohen: Coma, Dementias, Seizures, Syncope Flashcards
steps to take when found in coma?
- Stabilize: patent airway, adequate breathing, circulation
- Blood pressure and perfusion check: there may be circulatory collapse from hemorrhage or dehydration
- Peripheral or central intravenous line; draw blood for labs first, if possible; if any chance of hypoglycemia, give dextrose and thiamine
- Intubation/ventilation in many cases, sometimes just a cannula or a face mask for oxygen delivery; arterial blood gases can be followed
- Look for evidence of trauma, especially head and cervical spine
- Complete history from witnesses or neighbors or family; keep them available or get telephone numbers for later inquiries
- Comprehensive laboratories: chemistry, blood count, toxicology
- If any chance of opiate overdose, give naloxone (Narcan)
decerebrate vs. decorticate
decerebrate: (arm and leg extensions) is usually the top of the brainstem or the thalamus
decorticate: arms are flexed, legs extended - is usually widespread damage to both hemispheres
corneal reaction
blink reflex, is an involuntary blinking of the eyelids elicited by stimulation of the cornea (such as by touching or by a foreign body), or bright light, though could result from any peripheral stimulus.
tests CNs V and VII
oculocephalic reflex
normally vestibulo-ocular reflex results in eye moves in opposite way that head moves - if brainstem is in tact then eyes will do this
negative “doll’s eyes” are the result of eyes staying fixed midorbit = brainstem not intact
“Doll’s eyes” with eyes going opposite direction of head turn if there is NO inhibition by the cerebral hemispheres; rarely seen, because most coma patients have damage to brain AND both hemispheres, involving the pons and medulla oblongata
oculovestibular reflex
“cold calorics,”eyes deviate conjugately toward ear given ice water, involving the pons and medulla oblongata
hot water - eyes drift away from warm water
damage to CN III
see dilated, unreactive pupil and inability to move eye any dx except laterally (CN VI)
The nuclei for CN III are at the top of the brain stem, in the midbrain
The nuclei and its oculomotor fibers can be compressed by uncal herniation of the ipsilateral, and occasionally contralateral hemisphere
Brain damage without herniation also tends to hit CN III hard, causing weakly reactive pupils and both eyes tend to deviate laterally (again, if preservation of CN VI)
prognostic indicators for coma?
Probably the two most important signs:
- Pupillary reactions to light
- Spontaneous movements
Any patient with coma for 72 hours, excluding those with reversible swelling from trauma or sedation from drug overdose, or hypothermia, with multiple missing brain stem reflexes, has less than a 5% chance of a meaningful recovery
brain death
loss of brain stem and cerebral system
The patient who is brain dead IS LEGALLY DEAD
requirements:
- Exclude patients who may have a reversible condition: swelling from trauma, hypothermia, known drug overdose
- No evidence of cerebral function: no response to stimulation, no movements, no vocalization
- No evidence of brain stem function: all of the brain stem reflexes are absent, and no spontaneous respiration from centers in the medulla and pons
confirmation: APNEA TEST - – ventilator is turned off, but 100% oxygen is still delivered, until the PC02 rises to approximately 60 mmHg; if brain dead, no respiratory effort is seen at a high PCO2
other confirmatory tests: EEG, lack of cerebral blood flow on cerebral arteriography
Vegetative State
It suggests loss of both cerebral hemispheres, but maintenance of part or all of the brainstem
The brain stem can maintain sleep-wake cycles, respiration, heart beat, swallowing, some eye movements and facial contractions
Patients do not truly speak words but make some simple vocal sounds, such as grunts or event laughter
The arms and legs move but not in a directed manner
Gross vision is maintained, but no specific responses to what these patients seem to “see”
PVS = persistent vegetative state
definition: one month or more of vegetative state
- No awareness of self or surroundings, although eye opening and eye movements occur
- No meaningful communication between patient and others, including no comprehensible speech and no accurate mimicry
- Facial expressions not accurately related to stimulation, although patients may laugh or cry (CN VII in tact)
- Sleep-wake cycles may be intact
- Arm or leg movements, but not under voluntary control or with a directed purpose
- Adequate control of cardiovascular functions
- Incontinent of bowel and bladder
dementia def.
= loss of the “higher functions,” including memory, awareness, insight, judgement, executive function, abstract reasoning, visuospatial and construction skills, reasoning ability, social skills, use of meaningful language
- AD - 60-70%
- LBD/Parkinsons: 10-15%
- Multi-infarct/Vascular Dementia 5 - 10%
- Fronto-temporal Dementia : 5- 10%
- Alcoholism/Vitamin B12 deficiency: 5 %
AD
Pathogenesis:
- accumulation of beta-amyloid plaques
- accumulation of phosphylated tau protein in MT’s
- cell death, apoptosis - esp. in temporal and parietal lobes
** tau more effective in tx, thus maybe the more important accumulation.
seen in 10-25% of people 80+ y/o
Clinical Course;
- begins with a LOSS OF MEMORY for recent information or events - objects misplaced, trouble w/ names, repeating questions, speech restricted, trouble w/ daily affairs
- visuospatial decline, gait disorders
- depression, boredom, paranoia, anxiety
- apraxia - loss of simple actions
Levels:
- mild: ok at home, can be left alone
- moderate: pt. is kept at home w/ full-time caregiver
- Severe: pt. must go to nursing home
ddx:
- primarily clinical
- CSF shows tau increase and beta amyloid decrease
- brain MRIs show atrophy of medial and temporal lobe (but not specific)
tx of AD?
Option 1: AChE inhibitors: relieve memory impairement, agitated behavior by raising ACH levels - have a slower decline
- Donepezil (Aricept) Most widely used, well-tolerated, fewest systemic adverse effects, once daily
- Rivastigmine (Exelon) Strongly cholinergic effects, including vomiting and diarrhea, as a capsule, but now available as a skin patch to limit adverse effects
- Galantamine (Razadyne) Similar to rivastigmine, extended release form is available
Option 2: Memantine (Namenda)
- Antagonizes glutamate at the N-methyl-D-aspartate receptor
- May prevent cell death from glutamate activity
- Used alone or with an AChE for moderate or severe AD, but memantine is seldom very effective
Option 3:
Antidepressants are often needed, especially early in disease
There is often the use of antipsychotics to control agitation, anxiety; but studies show increased falls and earlier death
** keep pt. physically active and prevent from seeking isolation!
lewy body dementia
1/5 as common as AD
sx:
- dementia, agitated behavior along with decreased facial expression slowness and imbalance (but mild or no tremor) suggesting a case of early Parkinson’s Disease, except for the EARLY dementia and agitation, which are usually LATE problems in Parkinson’s Disease
- more common in men
- “crazy person” more psychiatric w/ parkinsonian mvmts - more angry/fear
common features:
- dementia, progressive but FLUCTUATING
- visual hallucinations
- parkinsonism - rigidity and slowness
tx:
* * BAD RESPONSE TO ANTIPSYCHOTIC DRUGS!!!
- may improve with AChE drugs
- levodopa sometimes given if parkinson sx increase
pathology:
- Lewy Bodies (alpha-synuclein seen in parkinsons) distributed throughout the brain NOT just substantia nigra.
- also have senile plaques and tangles
clinical course:
- more rapid decline than AD
- psychotic behavior fluctuates - may be injured or killed d/t hallucinations
multi-infarct dementia
- dementia d/t strokes causing ischemic changes –> rapid step-like downhill course
- “focal” findings on exam, including aphasia, dysarthria, hemiparesis, spasticity, visual field cuts
- Seizures more common than in other dementias
- Likely concurrent coronary artery disease, peripheral vascular disease and carotid stenosis, which may be seen with ultrasound
Common risk factors: HTN, DM, hyperlipidemia, obesity, smokers, alcoholics, CAD, A fib
tx: aspirin, anti-cogulants sometimes (warfarin)
fronto-temporal dementia
sx: decline in behavior and or speech - major PERSONALITY changes:
- apathy, bad behavior (these are bad guys! they care less)
- obsessive over certain things, overeating, drinking, junk food
- memory loss occurs much later in disease
- no auditory/visual hallucinations of AD
- equal in men and women
path: increased TAU, TDP-43 and UBIQUITIN (which normally removes waste products from cells)
contras from AD:
- vs AD which see temporal-parietal degeneration
- FTD is seen earlier around 50’s-60’s
ddx:
- NOT easy to make
- language decline is severe, can’t remember names
- shows other frontal sx: gait ataxia, clumsiness, poor decision making
- tx: none, though sometimes antidepressants and antipsychotics help
Broca’s aphasia
seen in FTD -
Primary progressive aphasia is a slow form of aphasia somewhat like Broca’s aphasia
The left frontal and temporal lobes have more atrophy than the right hemisphere
Sentences become shorter and shorter, with progressive inability to name, and read and write
Cruetzfeldt-Jakob Disease
CJD = transmissible spongiform encephalopathy
d/t infections w/ prions:
- Proteinaceous particles which can reproduce without nucleic acids, and change their molecular shapes from benign to pathologic
sx:
* ** rapid dementia in only 1 year *** also see prominent myoclonic jerks
- loss of balance, coordination
- very rapid downhill course
ddx:
- EEG shows triphasic waves
- CSF usually shows high levels of a 14-3-3 protein
- MRI shows rapidly accumulating subcortical deposits in the cerebral hemispheres, and cerebellar deposits sometimes
- brain biopsy shows spongiform changes
normal pressure hydrocephalus
- older pts. have lots of CSF d/t inability to reabsorb it
sx: “wide, wet, weird”
- gait disturbance, walks w/ small steps, incontinence, dementia, speech problems, walks with “magnetic” feet stuck to floor
- have normal opening pressure but see LOTS of CSF on CT
tx:
- May respond dramatically to ventriculo-peritoneal shunting
- Diagnosis can be strongly supported by the removal of 30 cc of CSF by a lumbar puncture
- This LP may cause a temporary clinical improvement for a few days, suggesting permanent shunting may be indicated
- Shunts may stop working eventually because of infection or blockage, or the patient develops other serious illnesses
syncope
= loss of consciousness from a lack of blood flow to the brain
- can be caused by anything that will cause drop in BP
Vaso-vagal syncope
“FAINT”
- caused by combination of:
1. sympathetic withdrawal (vasodilatation)
2. increased parasympathetic activity (bradycardia)
precipitated by:
- Hot or crowded environment, ETOH, extreme fatigue, severe pain, hunger, prolonged standing, emotional or stressful situation: Church services, funerals, military activities, athletic activities
- period of unconsciousness is usually less than a minute, and full recovery of consciousness occurs within five minutes
sx:
- pts. feel cold and sweaty
- pts. feel “light or woozy” , vision dims in both eyes, palpitations, “clammy feeling”, numbness
cardiovascular syncope
decreased CO (HR*SV) - bradyarrhtymia, tachyarrhythmia, left ventricular pathology, aortic stenosis, MVP, cradiomyopathy etc.
situational syncope
COUGH SYNCOPE: repeated coughing, especially in patients with chronic lung disease (COPD), may increase thoracic pressure and lower venous return to the right atrium; usually a brief period of LOC
MICTURITION SYNCOPE: elderly patients, almost always men who stand to urinate late at night, LOC due to the vagal response needed to urinate in patients who are sleepy; clinicians like to call this “Pee Syncope”
seizures
= : A widespread electrical discharge originating in the neurons of the cerebral cortex, causing an abrupt loss or decline in consciousness, new movements, altered bodily sensation, or unusual psychic feeling; perhaps in some cases by sub-cortical neurons
- Mediated by changes in ion channels, such as sodium, potassium and calcium, and by neurotransmitters, such as glutamate, and gamma amino butyric acid
epilepsy
= condition of two or more spontaneous (UNPROVOKED) seizures
- Epilepsy suggests a disease of brain function
Note: The majority of patients with a first seizure or even multiple seizures, will be found to have a cause, or provocation for this - Therefore, these patients are not truly epileptics, especially if the cause is temporary or can be reversed
two most common causes for provoked seizures?
- Hypoglycemia, which may also cause syncope
- Alcohol withdrawal: patients have one or a few seizures after being intoxicated, within the range of 7 – 72 hours, but typically less than 48 hours after they stopped drinking
Other causes:
- metabolic, fevers in chipdren, illicit drugs (cocaine methamphetamine), head trauma, brain tumors, brain hemorrhages, strokes
** every pt. w/ a first seizure should be evaluated, not every child needs an MRI, though EEG can be very helpful
generalized tonic clonic seizures
“grand mal seizures”
- often start in adolescence
- can be idiopathic or other cause
- tonic = increased tone, clonic = mm. start contracting and relaxing rapidly causing convulsions
clinical features:
- may experience “aura” at beginning
- first: tonic phase = clenching or tightening of the muscles in a fixed position, arms may be flexed, legs are extended, breathing muscles may be locked, and the mouth may close quickly causing biting of the tongue or lip and loss of urinary and rarely bowel continence
- The eyes often roll upward and should be OPEN at the start of the seizure
- Followed in approximately 10 – 30 seconds by the clonic phase, with repetitive synchronous movements of the arms and or legs
- seizure usually ends in two minutes, respiration resumes, pt. remains unresponsive for 5 minutes or more
physiologic changes:
- HR increases, O2 saturation drops, BP increases, pupils dilate, blood tests show metabolic acidosis
complex partial seizures
“Partial,” because they stay within one cerebral hemisphere
“Complex” because unlike partial motor or partial sensory seizures, the level of consciousness is partly reduced
- Very common, but not as easily diagnosed as tonic clonic seizures, even if there are witnesses
- Patients may get an aura more commonly than with tonic clonic seizures:
- Déjà vu: surroundings look strangely familiar
- Jamais vu: familiar surroundings look unfamiliar
Bad sensations such as an irritating smell or taste, a sense of dizziness, or an abdominal discomfort which rises to the head quickly
Clinical features:
- AUTONOMATISMS: I.E. LIP SMACKING, blank look, repetitive blinking, simple motion w/ hands, repetition of phrases
- can occur at any age, may be d/t trauma
- lasts one to two minutes
- and there is a post ictal period usually shorter than for a tonic clonic seizure
absence seizures
“petit mal”
- seizures in CHILDREN
- brief episodes lasting 10 seconds, less than 60 - resulting in inability to speak/respond and staring off into distance
- Patients do not fall down, except in atypical absence
- Occasionally blink or have repetitive movements of the face, eyes or arms
- Patients quickly recover a normal level of consciousness and do not even known they have had a seizure
- generally healthy children, often will lose this when become teens
** NOTE: EEG IS VERY DIAGNOSTIC! see three spikes every second
tx: valproic acid - depakote, or lamotrigine
status epilepticus
** A true medical emergency! can be fatal if not treated — 30 mins of seizing can cause permanent brain damage
Defined as:
- either multiple seizures without regaining of a normal level of consciousness between each one
OR:
One prolonged generalized seizure for 30 minutes (not including partial seizures)
tx:
- first check glucose, O2 levels
- stablize pt.
- the only time where IV benzodiazepines are indicated (have CI of respiratory arrest)
-
pseudoseizures
Some patients may unconsciously or deliberately have episodes which may appear to be seizures
Now more often referred to as Psychologic Nonepileptic Seizures, or PNES
Most of these patients have serious psychiatric illnesses, from conversion disorders to malingering, borderline personality disorders, history of physical and sexual abuse
- ** Look like generalized seizures, usually but with atypical features:
- ASYNCHRONOUS limb movements, eyes are often CLOSED, involve PELVIC THRUSTING or odd movements of the trunk, go on for more than 2 minutes, come on more slowly than typical seizures, do NOT respond to epilepsy drugs
