A neurology primer. Descriptions exist prior to Hippocrates Phrenitis ◦ Acute transient mental...
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Transcript of A neurology primer. Descriptions exist prior to Hippocrates Phrenitis ◦ Acute transient mental...
A neurology primer
Descriptions exist prior to Hippocrates
Phrenitis ◦ Acute transient mental disorder seen in
association with medical illness, with psychomotor agitation, insomnia and disturbances of mood/perception
Lethargus◦ Somnolence, inertia, reduced response to stimuli
An acute disorder characterized by disturbances in consciousness, disorganized thinking, fluctuating course with reduced ability to focus, sustain, or shift attention
Develops over a short time
Disturbances in cognition (memory, disorientation, perceptual/spatial disturbance)
Acute confusional state Toxic/metabolic encephalopathy ICU psychosis Organic brain syndrome Hepatic encephalopathy Beclouded dementia “Sundowning”
20% of hospitalized elders 50% of hip fracture patients Annual costs ~ $8 billion dollars Results in longer hospital stays, morbidity,
mortality, & nursing home placement 32-67% of cases never detected
Romano & Engel 1959 J Chron Dis
“The physician who is greatly concerned to protect the integrity of the heart, liver, kidneys of his patient has not yet learned to have the similar regard for the functional integrity of his patient’s brain”
A syndrome with cognitive, psychiatric, and neurological manifestations
Understanding the key elements of the syndrome is the most critical skill
Remembering “laundry lists” of potential causes is not useful
Read the nursing and therapy staff notes◦ Often the consult is literally done before ever
having to see the patient Listen to families & don’t tell them their
loved one is “back to baseline” if they state otherwise
Educate families & other medical staff
Hypervigilant◦ Frequently associated with drug
intoxication/withdrawal (delirium tremens) with increased arousal and autonomic lability
Hypovigilant or “quiet delirium”◦ Somnolent, sluggish, and apathetic
Mixed forms
A disorder of attention (ability to maintain a coherent stream of thought, free of interference from external or internal stimuli)◦ Sustained attention◦ Divided attention◦ Ability to inhibit irrelevant stimuli
Disorientation, poor memory, visuospatial disturbances & language changes are in large part due to disordered attention (unless they pre-existed due to underlying dementia)
Mood changes (depression, apathy, irritability, anxiety, & mania)
Psychosis is common!◦ Suspiciousness, paranoid delusions◦ Visual hallucinations
Delirium is the most common cause of new onset psychosis in the elderly
Asterixis Action or postural tremor Impaired postural control (balance) Bowel and bladder incontinence Motor tone abnormalities (gegenhalten type
rigidity)
The neuroanatomy of attention/arousal is diffuse & vulnerable at many points
Often the first to “fall apart” when elderly patients get ill for whatever reason
Precipitating cause is seldom “in the brain itself”, such as a new stroke, brain tumor, bleed, or CNS infection
CT scans, MRI scans, lumbar punctures are seldom useful and often red herrings
If you got one, look at it (brain size, vasculopathy, hippocampal atrophy, ventricolomegaly)
If you are completely unsure, then EEG is helpful but rarely needed
Delirious patients have decompensation of other processes that rely on widely distributed neural networks (maintaining the upright posture and continence)
Not surprisingly these recover together A person’s gait/balance may be just as good
an indicator of recovery from delirium!
Attention and arousal are dependent upon widely distributed neural circuitry and therefore vulnerable to a variety of insults
The neurotransmitters acetylcholine (ACh) and dopamine seem particularly important
Anticholinergic drugs cause delirium Cholinergic agonists reverse drug-induced
delirium Lewy body dementia mimics delirium Hypoxia, hyperglycemia, thiamine
deficiency cause decreased ACh release Alzheimer’s and other dementia at
increased risk Serum anticholinergic activity correlates
with delirium severity and incidence
Dopamine agonists can cause delirium Dopamine blockade treats delirium Dopamine release increases in hypoxia Dopamine is important in prefrontal areas Dopamine density in prefrontal cortex
decreases with aging and correlates with attentional measures
Distractibility Poor persistence Tangentiality and rambling incoherence Intrusions of irrelevant information
◦ Results in inability to learn new information, solve problems or engage in goal-directed behavior
“Patient is pleasantly confused” “He kept speaking of going to the
circus, & had difficulty following directions”
Patient stated “I want off this train. I am choking”
“Patient is very sleepy, and difficult to arouse”
Patient had a “rough night, was up all night and agitated”
Digit span forwards and backwards◦ Normal forwards is 7 +/- 2◦ Backwards usually 2 less than forward
Reciting overlearned tasks◦ Alphabet ◦ Months forward, days of week
forward/backwards
Counting 1-20 forwards, backwards Continuous performance task such as the
“A” test◦Raise and lower hand in response to letter A
Writing is extremely sensitive to delirium◦Draws on many complex skills and falls apart early
Document the mental status examination including description of cognitive/affective features◦ Record some test of attention (digit span,
counting span, months forward, alphabet etc.)◦ Describe mood/behavior (irritability,
hallucinations, paranoia, apathy, mood lability, sadness, etc.)
Document some neurologic exam (asterixis, action tremor, poor balance/instability)
Studies◦ CBC, CMP, urinalysis, pulse ox/ABG, EKG◦ Physical examination◦ Chest XRAY, other body imaging◦ Sometimes drug screen, tsh, b12/folate, thiamine,
lumbar puncture, neuroimaging◦ EEG can be useful in unclear cases looking for
diffuse slowing
Medications! (perform a detailed review) Common geriatric infections (pneumonia,
urinary tract infections, abdominal infections, cutaneous)
Hip fracture Metabolic disturbances (glucose, sodium,
calcium, acid-base) Hypoxemia CHF, myocardial ischemia
Furosemide 0.22 Digoxin 0.25 Warfarin 0.12 Nifedipine 0.22 Isosorbide 0.15
Ranitidine 0.22 Theophylline 0.44 Prednisone 0.55 Codeine 0.11 Cimetidine 0.86
Correct/remove all contributing factors Provide meticulous supportive care
(feeding, mobility, continence, pressure wounds)
Engage patient/family provide reassurance Correct sensory deficits (glasses, hearing
aids, avoid complete darkness) Falls alarm, sitter, family member
Avoid too much or too little stimulation Try to improve sleep/wake cycle Avoid iatrogenesis (physical restraints) Plan for discharge, follow-up and next level
of care Document your examination findings
Antipsychotics are first line Benzodiazepines only for alcohol or drug
withdrawal states Occasionally cholinesterase inhibitors may
be useful and are likely to play an important role as new research evolves
Avoid benzodiazepines except for alcohol/drug withdrawal◦ Haloperidol recommended first line for most
0.5 mg q 3◦ Avoid older sedating antipsychotics
(anticholinergic)◦ Atypical antipsychotics
Put on standing dose if requirement is frequent and supplement with prn
Goal is to treat cognition/psychiatric dysfunction, not sedation!
Haldol generally favored◦ Can be given IM, SQ, IV, PR, PO◦ Low doses in elderly frail patients 0.5 mg initially
and then every 4 hrs◦ Avoid in parkinsonian patients (need to recognize
EPS) Increasing use of “atypical antipsychotics”
◦ Olanzapine, quetiapine, risperidone, ziprasidone
Ensure not only medical but cognitive follow up as well
Document your exam for others Anticipate it will recur in the future and try
to optimize conditions so it will not Educate families about medications, and
the syndrome of delirium
Delirium is a common, costly and morbid condition
Delirium is fundamentally a disorder of attention
Delirium is poorly recognized Many patients have unrecognized pre-
existing dementia Many patients will ultimately develop
dementia