Neurological Disorders Part 1: MCCN FNP Primary Care 1

Neurological Disorders Part 1: MCCN FNP Primary Care 1


Hi, this is Christina Padrutt and this is
the lecture for neurological disorders I’ve broken this lecture into two parts
for you because there is a lot of content in this section. Part one of the lecture will contain information on confusion dementia, delirium, Alheimer’s disease, dizziness and vertigo, and headache. Part two will contain the information on paresthesias
and paresis, stroke, herpes zoster, tremor, multiple sclerosis, Parkinson’s disease,
and will end with some sample questions. Some of the common complaints that
you’ll get in primary care are: confusion, dizziness and vertigo, headaches,
paresthesias and paresis, and tremors so the objective of this section is to
discuss each of these in further detail. We’ll start the lecture with a
discussion on confusion. First and foremost, it’s important to remember that
confusion is a symptom. not a disease process. Confusion is the inability to
think clearly or coherently. The patient may be disoriented to person, place, time,
and/or situation. Neurological and cognitive dysfunction are demonstrated
by inappropriate reactions to environmental stimuli, and the onset can
be either sudden or gradual and may be temporary or irreversible depending on
the cause. While age is not a predictor of
confusion elders are most at risk for confusion due to multiple factors such
as polypharmacy, the aging process, and the presence of chronic diseases. Here we
have the flowchart for the differential diagnosis for confusion which is found
in 6.1 in your textbook. Please review this further, but we will also discuss
this flowchart. Diagnosing the cause of the confusion starts with a thorough H&P.
Your history of present illness should include signs and symptoms, your
OLD CARTS, make sure you’re monitoring vital signs, pulse oximetry, a thorough
neurological exam should be performed. There are multiple screening tools such
as the FAST, MoCA, and the MMSE, which we’ll discuss in further detail. A good point
for your starting assessment with lab work is a comprehensive metabolic panel,
hemoglobin a1c, TSH, UA, and a drug screen. This is kind of your
basic recipe for beginning your evaluation of the patient with confusion.
And, of course, you’ll want to do a thorough medication review- as multiple
medications can cause confusion as a side-effect. One of the first groups that
should be in your differential diagnosis for the patient with confusion is
metabolic cause: either fluid or electrolyte or acid-base imbalance. These
can be caused from a disturbance in the renal system, hepatic system, uncontrolled
diabetes, thyroid disease, nutritional deficits, hypo or hyperthermia, or
hypoxemia related to a vascular or pulmonary process such as CVA, MI, CAD, CHF, or COPD. Then next on our differential diagnosis, should be looking at
infectious process as infection can also lead to mental status changes. So, you’ll
want to evaluate is there possibly a pneumonia, a UTI, encephalitis, meningitis,
brain abscess or sepsis. Neoplastic processes can also contribute to mental
status changes, especially if the brain is involved. The next thing you want to
consider is toxicology. Is the confusion related to drugs or alcohol? And when
evaluating for drugs, don’t forget about street drugs, even in
the elderly population. That population- we are seeing opioid abuse and illicit
drug use. Then of course the prescription medications- you want to
consider is it a polypharmacy issue? Are they on too many medications? Are there
medications interacting with each other? And then miscellaneous- anxiety, or
environmental. And then the next thing you want evaluate is, could it possibly
be a delirium or a dementia? It’s important to remember that
these are separate processes although there is some overlap at times. It’s
important for the practitioner to be able to differentiate between delirium
and dementia. One should be able to compare and contrast: the onset, timing,
duration, causes, symptoms, screening tools used, treatment, and prevention or
follow-up care for each. We’ll discuss that further in this lecture. So,
if you’ve ruled out the other causes (such as metabolic, infectious, and hypoxemia) and you’re pretty sure that you’re dealing with a delirium versus dementia,
then the main concern with the differential diagnosis for the confusion
is to determine if the symptoms reflect delirium, dementia, or possibly delirium
superimposed on dementia. Once everything else has been ruled out. So let’s start
with the discussion of dementia. Dementia is a decline in mental functioning
affecting one’s memory, cognition, language, and personality. The onset is
slow, occurring over months to years, and the timing is a subtle decline. Dementia
tends to have a very insidious onset. The symptoms are lifelong but there is a
significant time span between symptom onset and death generally speaking. There
are multiple causes of dementia. These include, but are not limited to:
Alzheimer’s disease, Parkinson’s disease, vascular dementia, metabolic or endocrine
disorders, trauma, and infectious diseases. The initial symptoms shown are cognitive
defects: aphasia, apraxia, and/or agnosia and may cause impaired occupational and social
functioning. Patients demonstrate disturbances in planning, organizing,
sequencing, and abstracting. Symptoms progress in severity including
incontinence, inability to do ADL’s, inability to speak, and progressive weight
loss. Diagnostic testing includes the Mini Mental State Examination (or the
MMSE), the SLUMS evaluation, MoCA and the FAST (functional assessment staging) and
we’ll talk a little bit more about these in further detail. Let’s start with the MMSE, as in my experience this is the most commonly
used evaluation tool. The MMSE has a total possible score of 30, and a score
of greater than 24 is considered unremarkable. 21 to 24 is indicative of
mild dementia. 13 to 20 indicates moderate dementia and a score of less
than 12 indicates severe dementia. According to Alzheimer’s org, for example, in a patient with Alzheimer’s, you can expect to see a 2 to 4 point per year
decline and the MMSE score. That’s why it’s important to document the MMSE
and keep a record of it in your patients chart over time. Treatment for dementia
should be disease and symptoms specific. For agitation or anxiety, first you want
to try some behavioral management strategies but if those are not
successful antidepressants can be helpful, also anxiolytics and antipsychotic medications such as haloperidol quetiapine, priperidone, olanzapine, and aripiprazole: but you want to monitor EKG changes for QT elongation and we’ll talk
a little bit more about use of antipsychotics in the patient with
dementia and sort of the cautions that come along with that.
For impulsivity and aggression carbamazepine can be used. Cholinesterase inhibitors are frequently used, and again, tying in behavior management, caregiver
respite, and cognitive stimulation are also very important tenets of treating
the patient with dementia. Now let’s switch our focus to delirium. Delirium by
definition is an acute fluctuation in attention mental status and level of
consciousness. And again, it’s very important to distinguish dementia from
delirium and you may have delirium superimposed on dementia so it’s very
important to remember acute fluctuations because that will be
one of the keys in distinguishing these two processes. There are some
common characteristics and causes however, and once the cause of delirium
is corrected the patient should return to baseline neurological functioning
while in dementia the patient will not due to dementia being a chronic disease
process. So the onset for delirium, again, its abrupt ,acute, and can occur within
hours to days. The confusion fluctuates throughout the day the patient may be
oriented one time you see them and then if you see them a couple hours later
they may be very very confused. It can last hours two weeks. Causes of delirium include: stroke, an acute medical condition (for example HH
NKS), urinary retention, constipation, sensory deprivation, fever or infection,
polypharmacy, hypoxemia, metabolic derangement, or surgery. Symptoms include inattention, sleep disturbance, memory loss, psychomotor retardation or
agitation, hallucinations, language disturbance, and stupor. The
MMSE can be used as a screening tool for delirium as well to evaluate the
severity of the cognitive impairment. Teatment for delirium: the number one
treatment for delirium is to treat the underlying cause, and again, once the
underlying cause is treated the delirium should resolve and the patient should
return to normal baseline cognitive function. Make sure you have sensory aids
available for your patients such as glasses/hearing aids. Keep them on a good
bowel and bladder regimen. Make sure their bladders emptying, and make sure
they’re having bowel movements. Have them up for meals, encourage familiar people
and objects in their environment, avoid or minimize polypharmacy as much as
possible, reorient the patient, safe mobilization (as they may be fall risks
especially in the setting of delirium- but they still need to be mobilized ), so
whether that be with a family member or some sort of therapy, mobilization is important. I want to emphasize that non
pharmacological interventions are the gold standard of treatment for delirium
by evidence. Antipsychotics may be used for agitation, however, they should be
used at the lowest dose. They should be short acting medications and only used
if absolutely necessary if the patient’s demonstrating psychotic behaviors or
[moderate] to severe agitation that’s putting staff, family, or the patient in danger.
Avoid benzodiazepines. I know a lot of times staff will call and request Ativan for a confused patient. This is not the standard of care. Benzodiazepines
can cause paradoxical agitation and adverse effects, especially in in the
elderly, including increased risk of falls. Now we’ll discuss some of the
situations in which the patient exhibiting delirium should probably be
treated in an inpatient setting or at least evaluated in an emergency
department. Keep in mind that we’re looking at this through the lens of
primary care and we’re looking at these things in the lens of the patient
who’s exhibiting delirium. So: metabolic disturbances, such as
hyponatremia (moderate to severe, which is a sodium of 130 meq/l
or less) should be evaluated. Once in an acute care setting, they’ll determine
the type of hyponatremia to guide the treatment. It’s very important to know
why they’re hyponatremic so you can give them the proper treatment. Hyponatremia can be
hypervolemic, hypovolemic, or euvolemic. Fluid restriction and diuresis would be the
treatment if they are hypervolemic. Sodium chloride administration would be the treatment if they are hypovolemic, however, this should be done with extreme
caution as locked-in syndrome (or pontine demyelinating syndrome) may occur if the
sodium is corrected too rapidly. You never want to bolus a patient who is
hyponatremic from hypovolemia. Start very slowly with your IV fluids. Sodium should
not be corrected more rapidly than six meq/l per 24 hours. If SIADH
is the cause of euvolemic hyponatremia, the patient may require interventions
such as ddavp and should also have further evaluation for causes of SIADH.
Keep in mind you can also have pseudohyponatremia in the setting of
hyperglycemia. There are sodium correction calculators available online
that are very useful in practice. Another metabolic disturbance that
warrants inpatient evaluation is metabolic acidosis. There are many
forms of metabolic acidosis, in particular DKA, sepsis, and lactic acidosis.
Depending on the cause, that would guide treatment. Again, in the setting of
DKA – they may need IV hydration, IV insulin, and a DKA protocol in including
frequent chemistries for hypokalemia, hypophosphatemia, anion gap, and glucose. For dehydration, fever, and sepsis that require large volume fluid resuscitation.
Infectious disease workup including blood cultures, urine cultures, chest
x-ray, and broad-spectrum antibiotics and with sepsis protocol, these things are
expected to be done within a certain time window. If you’re working in an
inpatient setting, you’ll learn more about that in practice so we won’t go
too far into that since the the lens we’re looking through is primary care. The bottom line here is send them to have an inpatient evaluation. Again,
looking through a lens of primary care and the patient with acute mental status
changes, hypoxemia would warrant a trip to the emergency department. Hypoxemia
could be caused from cardiovascular issues due to ischemia from a stroke,
atherosclerosis, heart failure, aortic or mitral insufficiency, or cardiac
arrhythmias. It may also be from pulmonary causes such as: COPD exacerbation,
pulmonary hypertension, pulmonary embolism, or ARDS. Neoplastic diseases,
brain tumors, paraneoplastic diseases: if you are suspicious of this causing their
mental status changes, send them for an evaluation and workup.
And of course for stroke you’d want to make sure that your patient is sent immediately
to the emergency department. All right, now let’s discuss Alzheimer’s disease.
Alzheimer’s disease is a progressive neurodegenerative condition with an
insidious onset with slow progressive cognitive decline and emotional and
behavioral problems. It’s the impaired ability to learn new
information or recall previously learned information; and additionally one of
these cognitive disturbances are also present: trouble with language (or aphasia),
function (apraxia), perception (agnosia) or executive function. Again: language,
function, perception, or executive function will also be affected. There are
different forms of Alzheimer’s disease. Alzheimer’s may be familial or sporadic. In the case of genetic mutation, this is
a sporadic form of Alzheimer’s disease where the risk is increased with age,
lower educational and occupational levels, family history, head injury, Down
syndrome, and decreased estrogen levels. In the familial form:
it’s a genetic transmission from the parents and you can differentiate these
in that in the familial form, the onset tends to be earlier. Clinical manifestations of Alzheimer’s disease: on the subjective part of your assessment
your patient (or their family) may complain of memory problems, getting lost
in familiar places, the inability to accomplish a demanding task at work that
they’ve previously been able to do, slow response to any cognitive challenge,
difficulty word finding especially with words that they have previously not had any
trouble with, difficulty with routine tasks (such as balancing the checkbook
cooking dinner traveling or maintaining employment). This progresses to problems
with simple tasks such as choosing clothing, doing housework, eventually
progresses to needing help with their ADL’s and may also include behavioral
problems such as hostility, aggression, suspiciousness, paranoia, delusions,
agitation, or impulsive sexual behavior. Remember that there’s a fine line
between the benign forgetfulness of age associated memory impairment and the
onset of Alzheimer’s disease. Some of the keys are: word finding difficulty
otherwise known as anomia, trouble during routine chores, and that the symptoms
progress to experiencing difficulty with simple tasks and up to performing ADL’s.
Cognitive assessment is central to the diagnosis of Alzheimer’s
disease. MMSE, (which we’ve already gone over you
can refer back to the previous slide on that), MoCA is the Montreal cognitive
assessment: similar to the MMSE but less complex to administer. FAQ: functional
activities questionnaire- evaluates the ability to perform ADL’s and it’s good
to use as a baseline. The timed to get up and go test, and simple testing such as:
having the patient draw a clock with the time, write a sentence, ask them what they
had for breakfast that morning, or what they did last Sunday. Save these
evaluations in the chart and repeat over time for comparison.
In addition to your screening tests, you’ll want to get a focused history.
Going through your OLDCARTS, family history, a thorough neurological exam
(make sure you’re looking for delirium causes and that this is not just a
simple delirium as opposed to chronic dementia such as Alzheimer’s), you’ll want to make
sure you consider age, visual and auditory impairments, and educational
level when interpreting the cognitive test results. Some lab tests that you’ll
want to include in your workup include: CBC, CMP, TSH, ammonia, and hemoglobin a1c, a
non-contrast CT of the brain or an MRI of the brain may be considered to rule
out surgically treatable lesions and vascular disease. There’s also the
Pittsburgh compound B PET scan which can detect amyloid deposits.There’s
current ongoing research for biomarkers in the blood to screen for Alzheimer’s
disease. These look for the accumulation of beta amyloid in the brain and neuron
degeneration. These may become important for screening for diagnosis
and monitoring response to treatment in the future. The value of genetic testing
remains controversial, as is the the whole concept of direct-to-consumer DNA
testing which can give patients information on SNPs as to whether or not
they carry some genetic markers for alzheimer’s disease. We could get
into a whole ethics conversation about direct-to-consumer DNA testing, but we’ll
save that for another day. Just be mindful that patients may come to you
with questions if they’ve taken any of this direct-to-consumer testing that’s
given them any information on their risk for for dementia or Alzheimer’s in
particular. This graphic is from your book on page 110, and it’s the assessment
of Alzheimer’s disease. Next, we’ll discuss the differential diagnosis which
follows along with the infographic. Remember your differential
diagnosis begins with the process of excluding other causes of cognitive
impairment. You’ll want to rule out medical conditions and drug related
adverse effects such as: infection, structural CNS conditions, trauma,
metabolic or organ failure, and anemia. You’ll also want to consider: depression, drug
abuse, psychosis, mental retardation, whether or not there’s alteration in
LOC, or if this is a delirium process. It’s important to remember that the
differential diagnosis for Alzheimer’s disease is still a process of excluding
other causes of cognitive impairment including medical conditions, and drug
related adverse effects, infection, structural CNS conditions, trauma,
metabolic or organ failure, anemia, depression, drug and alcohol abuse,
and psychosis. You’ll want to rule out mental retardation and if there’s no LOC
change then that rules out delirium. Amnesia and aphasia need to be
considered if there is multiple cognitive functions that are impaired.
For a chronic presentation, you’ll want to rule out Creutzfeldt-Jakob disease,
tumor, b12 deficiency, drug intoxication, and metabolic disorders. If there’s a
steady decline rather than a stepwise decline consider vascular dementia. Also
consider primary cortical dysfunction: rule out Parkinson’s, Huntington’s, again,
trauma, and vascular dementia. Depression can mimic Alzheimer’s disease and this
is known as pseudodementia which is a frequent misdiagnosis in elders. In this
case, you would want to treat the depression first for a few months and
then reassess the patient by repeating cognitive testing. Some things that would
give you a high index of suspicion for Alzheimer’s disease include the absence
of precipitating medical illness, the
absence of drug-related conditions, the presence of objective well-documented
progressive and worsening deficits in new learning and memory which is
documented through cognitive testing such as the MMSE and recorded in the
patient’s chart over time, and also, if there are signs of functional impairment.
Principles of management for Alzheimer’s disease are aimed at slowing the
progression of the disease and we do this through medications protecting the
overall physical health, by eliminating modifiable risk factors such as smoking
drug or alcohol use, providing emotional support (not only to the patient but to
their caregivers), maintaining maximum function, and maintaining normality in
their relationships. Patients and families need assistance in
understanding the disease and coping with the diagnosis. Support groups can be
very helpful- but they must be relevant to the stage of the disease. It’s
very important, again, to treat depression and anxiety because these often lead to
aggression and other problem behaviors seen in dementia. Next we’ll discuss
medication therapy and Alzheimer’s disease: for mild to moderate Alzheimer’s
disease, usually started at time of diagnosis, is the cholinesterase
inhibitors. These include medications such as donepezil, galantamine, and rivastigmine. For moderate to severe Alzheimer’s: NMDA receptor agonists such
as memantine are used. These can be used alongside cholinesterase inhibitors
however you need to keep an eye on your patients creatinine clearance with renal
impairment as they may need a dose adjustment. These do require several
weeks to show efficacy. Anxiolytics such as buspar can be used to help control
anxiety symptoms and again atypical antipsychotics only if absolutely
necessary. You want to limit the use of these due to side effects.
Use with caution aa they do carry a black box warning for increased risk of
death in the elderly population. These medications include risperidone: which
you would want to avoid in vascular dementia because it may increase the
risk of stroke, olanzapine: you’ll want to avoid alcohol
because it can increase CNS depression, and quetiapine. Alright, on to dizziness
and vertigo. So, just a quick review of dizziness and vertigo: dizziness is the
sensation of unsteadiness lightheadedness or weakness while
vertigo is the false sensation of movement (often but not always rotation
or spinning of the patient or the patient’s environment). Loss of
consciousness rarely occurs. As a clinician it’s important to distinguish
between dizziness and vertigo. Dizziness is brief and may be mild to severe with
abrupt or gradual onset usually caused by inadequate blood flow and oxygen
supply to the brain and spinal cord, whereas vertigo is usually an inner-ear
issue, vestibular center or CNS disorder. If it is associated with symptoms of
numbness, facial, arm, or leg weakness you should suspect a brain stem problem. 44%
of dizziness and vertigo is caused by a peripheral vestibular disease which is a
disease of the vestibular nerve. It’s a common pathology that precipitate in the
labyrinth of the middle ear causes disequilibrium. Clinical manifestations
include dizziness, nausea and vomiting, diaphoresis, difficulty with balance,
vertigo, tinnitus, fluctuating hearing loss, a feeling of pressure in the ear,
and possibly double vision. This is diagnosed through audiological
evaluation ENG MRI MRA and brainstem evoked responses.
Labs and physical examination: treatment of peripheral vestibular disease
includes antihistamines such as meclizine diphenhydramine or
promethazine- which suppress the vestibular receptors
therefore inhibiting the action of the vagal responses. Antiemetics are good
adjunct therapy for nausea and vomiting. And physical therapy, for vestibular
exercises to help dislodge the otoliths, decreasing the duration of vertigo and providing longer symptom-free periods between
exacerbations. To do this maneuver you will place the patient’s affected ear
down then assume a supine position and hold that position until the vertigo
disappears. The vertigo may return when the patient sits up, and the maneuver
should be repeated approximately five times a day. Dizziness and vertigo may be
caused by systemic disorders. These disorders: may cause dizziness,
lightheadedness, or syncope; can be aggravated by postural changes or
exertion. Clinical manifestations may include pallor, dyspnea, tachycardia,
bounding pulse, weakness, hypotension, blurred vision, headache, diaphoresis,
decreased breath sounds, and/or agitation. In this case, if you’re suspecting a
systemic disorder, your differential should include: anemia, cardiovascular
disease, hyperventilation, drug reaction, endocrine disorders, fluid and
electrolyte imbalances (such as dehydration), and psychiatric problems
such as anxiety. Dizziness and vertigo can also be caused by central nervous
system disorders which disrupt the pathway between the vestibular apparatus
and the brain leading to dizziness. Clinical manifestations of CNS disorders
include facial numbness, hemiparesis, diplopia, dysarthria, headache, and nausea
and vomiting. In the next slide we’ll review flowchart 6.2 from
page 82 in your textbook for the differential diagnosis of dizziness and
vertigo. Feel free to take a moment to pause this presentation and zoom in on
this flow chart or refer to your textbook: again this image is on page 82. Dizziness is classified into four
categories including peripheral vestibular disease, systemic disorders,
CNS disorders, and anxiety or psychiatric states. In obtaining your history and
physical there are some key questions you want to make sure to ask about the
duration, severity, and nature of the episode, and also any associated symptoms-
especially hearing loss or weakness. You’ll want to do a thorough autoscopic
exam to rule out cerumen impaction, otitis media, (some of the more simple things).
You’ll want to perform a hearing test such as whisper test and the Weber and
Renne tests and do a complete neurological assessment. To distinguish
between benign vertigo and vertigo resulting from a CNS lesion, the Dix-Hallpike maneuver is used. To do this maneuver you’ll want to rotate the
patients head to one side and lower it slowly to 30 degrees below the body line.
There is a graphic of the Dix-Hallpike maneuver on the next slide. You’ll then
want to observe the patient for nystagmus and vertigo that resolves when
the patient is sitting up again. Nystagmus should be limited and cannot be reproduced in BPPV (which stands for benign paroxysmal
positional vertigo) However if there is a CNS lesion, the vertical nystagmus is
persistent and can be repeated. Here you see a graphic demonstrating how to
perform the Dix-Hallpike maneuver as described on the previous slide. For our next topic we’ll cover headaches. Remember that about 90% of headaches
have no pathological cause. There are four general categories of headache:
tension headaches, migraine and cluster headaches, mixed headaches (which are a
combination of the first two), and traction or inflammatory headaches. Muscle
contraction headaches (or tension type headaches) make up more than 50% of the
pathological headaches. These can be either primary (without an underlying
cause) or secondary headaches (the result of trauma, infection, arthritis, or tumors).
Tension type headaches are most common in young female adults and can be
associated with anxiety and depression. Vascular headaches include migraines and
cluster headaches. Mixed headaches are a combination of muscle
contraction and vascular causes. Traction or inflammatory headaches are the most
concerning. These tend to be abrupt explosive headaches described as the
worst headache of the patient’s life and these are often due to intracranial
hemorrhage. These are considered emergent. Next we’ll talk a little bit about
headache pathophysiology remember that only certain structures in the head are
sensitive to pain due to pain receptors and these are the dura between the
cerebral hemispheres the middle meningeal artery of the dura the dural
sinuses which is part of the venous system in the head and the pial arteries
on the surface of the brain. Increased pressure or inflammation can put
traction on the arteries leading to the sensation of pain. As I mentioned before
there are primary and secondary headaches. Primary headaches are tension
type headaches migraines and cluster headaches.
These require the hyper sensitization of the trigeminothalmic
and cervicothalmic circuits when the pain stimuli passes through the thalamus
the signals are modulated by an abnormal reduction of serotonin activity hence
the reason for the effectiveness of serotonin agonist otherwise known as the
triptans which can reduce pain and frequency of migraines and reduce the
duration and frequency of cluster headaches SSRIs may also be used to
reduce the frequency of tension type headaches. Secondary causes of headaches,
so in other words other processes that are the cause of the pain include head
trauma intracranial hemorrhages ischemic stroke intracranial infections tumors
metabolic disorders such as hypercapnia hypoxia and hypoglycemia sudden
hypertension increased intracranial pressure drugs and drug withdrawals
cranial nerve pain and ear eye nose sinus teeth and jaw disorders can all be
secondary causes of headache. For secondary headaches the pain signals are
transmitted by the trigeminal nerve to the anterior head face and jaw. Pain
signals for the posterior head are transmitted by cervical spine nerves c1
through c3. In the first order pain fibers from these nerves synapse in the
brainstem and upper spinal cord. From there the second order pain fibers
project to the sensory nuclei in the thalamus.
Therefore the headache pain is caused by activating these trigeminothalmic and
cervicothalmic pain circuits. Next we’ll talk about some more specific
types of headache. We’ll discuss tension headaches. For tension headaches you’ll
find this typical presentation: the patient will complain of mild to
moderate bilateral non pulsating tightening type pain.
Bilateral head tightness last 30 minutes up to a week.
It is not aggravated by routine physical activity, not associated with nausea
vomiting or photophobia. Tension headaches tend to come on gradually
during the day and are more common in patients with depression. Tension
headaches are the most common type of headache. This is a primary headache more
often seen in women. Prevalence peaks between ages 30 and 38 more frequent in
whites with higher education levels and may affect your patient by causing
decreased effectiveness at work home or school. A quick overview on migraine
headaches: migraine headaches are the second most common type of headache.
African-americans in Latinos are twice as likely to have migraines compared to
whites and Asians. The highest incidence being in younger
adults under the age of 40 and lowest and adults over the age of 60. They do occur
in four to five percent of school-aged children and can often be hereditary
caused by mutations in calcium channel genes. The presentation of migraine
headaches: there’s usually a predictable pattern starting with a prodrome which
could be hours or days before the actual headache. Some patients experience
psychological change such as drowsiness depression euphoria hyperactivity
difficulty concentrating irritability or increased sensory perception. Migraines
tend to be unilateral moderate to severe in intensity with a pulsating quality.
Often accompanied by nausea and vomiting heightened sensitivity to light smells
and sounds and occur repeatedly one to three times a month and can last four to
72 hours. Migraines often have triggers the most common being alcohol stress
menstruation or diet. A little bit more about migraine triggers the migraines
are triggered by hormonal shifts and women before
during or after menstruation. There can also be environmental triggers including
high-pitched noises sunlight bright lights weather changes strong odors
video displays. Diet can affect migraine in various ways.
Vasodilating agents such as alcohol or sodium nitrate can bring out a migraine
as can vasoconstricting dietary agents such as caffeine, bananas, ripe cheese,
nuts, broad beans, chicken livers, yogurt, avocado, or sour cream.
Phenlethylamine found in cheese red wine and chocolates can also be a
migraine trigger, msg found in chinese food canned soup and frozen dinners,
artificial sweeteners, stress, exertional sports (such as swimming cycling
weightlifting), sun tanning, fatigue, dehydration, changes in sleep schedule,
and smoking can all be triggers for migraine headache. In the classic
migraine the headache is preceded by a sensory phenomena called an aura a set
of patterns in the visual fields or sensations that move from the hand up
the arm to the face. The aura coincides with a wave of chemical activity that
moves across the cerebral cortex. As the wave reaches a region it briefly
activates the neurons and increases the local blood flow. After the wave passes
it leaves the neurons refractory and the local cerebral blood flow decreases. The
wave contributes to the hypersensitization of the trigeminothalmic circuits
and elicits the pain perception of the headache. So the basis for the pain and
migraine headaches is a hypersensitive trigeminothalmic circuit which makes the
pulsing of the cerebral blood flow feel painful. This hypersensitivity can carry
over to all of the trigeminal nerve branches on the same side of the head so
that normal pressure is on the skin of the face and scalp can feel painful.
In addition to the triptans other drugs used in treatment of migraine include
adrenergic agonist such as norepinephrine alpha-2 agonist such as
clonidine and beta blockers such as propranolol can stop or slow this wave
of cortical depression. As an epilepsy migraine headaches have
cortical neurons that are permanently hyperexcitable and this can be
inherited. Cluster headaches are another type of vascular headache. They’re named
cluster headaches because of the pattern of occurrence. They’re usually grouped
over several weeks to months. They will then disappear for months or even years
only to recur again. Cluster headaches are often on a seasonal basis for the
sufferers.These are considered the most painful types of headaches and often
occur in middle-aged men. This is caused by a dysfunction of the hypothalamus
which may account for the regularity of the headaches. Cluster headaches are triggered by an
abnormality in the ipsilateral circadian pacemaker which is located in the
ventral hypothalamus. The pain is then caused by hypersensitization of the
ophthalmic nerve, a branch of the trigeminal nerve. The autonomic symptoms
are caused by concurrent excitation of parasympathetic fibers that run with the
ophthalmic nerve. Cluster headaches come in groups that last two to three months.
They occur at night and may last 15 to 180 minutes on average. They tend to be
severe unilateral in the orbital super orbital and/or temporal areas. They are
accompanied on the same side of the face with sweating lacrimation nasal
congestion ptosis rhinorrhea eyelid edema and/or conjunctival injection.
Cluster headaches radiate to the forehead neck or shoulder, do not pulsate,
are not associated with nausea and vomiting, and are not aggravated by
activity. Traction or inflammatory headaches occur secondary to systemic
disease or a primary intracranial lesion such as a subarachnoid hemorrhage from AV malformations or aneurysms. Other causes
include temporal arteritis or subdural hematoma. Temporal arteritis is
predominantly seen in older adults over 60 and as an inflammation of the
temporal artery subdural hematomas are usually from trauma and are venous
bleeding they occur predominantly in people over 50 and are more common in
men there is an increased incidence in subdural hematomas with alcohol abuse
and use of anak coagulants however the skull is rarely seen to be fractured
with subdural hematomas subarachnoid hemorrhages 66% of subarachnoid
hemorrhages are seen in individuals aged 40 to 60 with women slightly more often
than men subarachnoid hemorrhages are usually from the rupture of a cerebral
aneurysm or an AV malformation av malformations are usually congenital
vascular malformations an aneurysm is a weakened artery wall that balloons out
whereas an AVM is the connection of an artery and a vein without the
intervening capillaries activities such as lifting straining sexual intercourse
or emotional excitement can precipitate a subarachnoid hemorrhage traction or
inflammatory headaches often present as acute new onset headaches that have an
increasing intensity if you’re patient demonstrates symptoms of a subarachnoid
hemorrhage or an infection such as meningitis this is considered a medical
emergency and they should be directed immediately to the nearest emergency
department moving on to diagnostic testing for
headaches pretension type or migraine headaches or no change in the headache
pattern EEG CT and MRI are not recommended however you can do lab work
to rule out systemic illness including a CBC BMP and UA if you suspect temporal
arteritis ESR CRP may be normal and you should refer the patient for temporal
artery biopsy CT or MRI may be indicated if the
headaches are an atypical pattern if there are change in the headache pattern
or if there’s accompanied by seizure personality change or abnormal
neurological findings CT is useful for screening for subdural hemorrhage for
example while MRI or MRA can look for hematoma and tumors and I supplied a
link on this slide for the headache classification system of the
International Headache Society that can be found at HTTP colon forward slash
forward slash IC hd3 dot org and if you have a few minutes logon there and it
has a lot of good information on headaches
that you might find useful while studying this section as well so the
headache classification committee of the International Headache Society came up
with an operational diagnostic criteria for 14 headache categories for example
the diagnostic criteria for migraine without aura includes two of the
following unilateral location pulsating quality moderate to severe intensity and
exacerbated with physical activity and at least one of the following nausea and
vomiting photophobia or phony phobia in here we have an algorithm for the
differential diagnosis for headache take a moment to pause this presentation zoom
in and review these slides but we will discuss this in the next few slides as
well as usual you’ll want to start with the good history of present illness
noting the onset location frequency duration severity character presence or
absence of aura whether or not there’s an association with sleep or emotional
factors precipitating and leaving factors in family history when
evaluating headache you’ll want to assess that there’s been any sleep cycle
disturbances if there’s depression have there been
appetite changes are there relationship or job difficulties recently remote
memory loss and whether or not there’s limited range of motion of the neck
getting a good history is essential to distinguish headache syndromes from
life-threatening event such as subarachnoid hemorrhage or stroke
besides the past medical history don’t forget to get a good social and family
history as well when getting the review of systems remember to check for history
of head or neck trauma medical procedures that could have contributed
to headaches such as lumbar puncture spinal anesthesia or other surgeries for
example bilateral headache may develop seven days following a lumbar puncture
the headache typically worsens with standing and is relieved by laying down
within 30 minutes there can be other causes of headaches
such as recurrent medical conditions such as hypothyroidism hypertension and
asthma certain medications may also provoke headache
remember the sudden onset of pain may suggest a serious pathology such as
subarachnoid hemorrhage meningitis or brain tumor
headaches that have been present for years are more likely migraine cluster
or tension type headaches and the character of the pain and associated
signs and symptoms can be great great to help differentiate between the different
types of headaches identify programs and auras or the absence of into a complete
comprehensive neuro exam including motor strength and sensory testing again
warning signs for secondary problems such as progressive headaches that
worsen over time the worst headache of my life new onset headaches over 50
persistent headache precipitated by valsalva maneuver x’ fever hypertension
myalgias weight loss or scalp tenderness neurological signs and symptoms such as
confusion altered LOC changes in memory papilledema sensory deficits reflex
asymmetry or gate disturbances and seizures again you’d want to do a
thorough investigation if you have these warning signs of secondary headaches
headache management for tension headaches and said such as aspirin
acetaminophen Aleve triptans for chronic tension headaches these can also be used
for prophylaxis cool compresses stress reduction for the treatment of migraine
headaches non pharmacological intervention eliminate triggers if
they’re known maintain a schedule for sleeping and eating used biofeedback and
meditation relaxation techniques and aerobic exercise aboard of therapy with
triptans pain relief with aspirin naproxen ibuprofen and prophylactic
treatment with propranolol metoprolol verapamil gabapentin and lyrica or
topamax you know identify therapeutic goals with your patient which may
include strategies to avoid triggers discuss the their ability to abort a
headache and what they’re going to do for that ways to obtain relief from the
pain and associated symptoms as well as decreasing the frequency and the
severity of their headaches when they do occur you’ll want to make sure that
you’re doing good patient education setting realistic expectations patient
education should include the causes of their particular headache patients
should be encouraged to keep a headache diary trying to identify triggers and
treatments that are most effective exogenous triggers such as food for
example red wine alcohol cheese msg artificial sweeteners chocolate lights
oral contraceptives or environmental triggers such as stress air travel
weather changes and odors patients should be encouraged to warm up before
exercise to avoid straining muscles that could contribute to headache avoid
tight-fitting glasses goggles helmets and hat
and you should discuss birth control methods before treating headaches and
the patient should be educated to let the provider know if they become
pregnant stress management should also be included in your management strategy
this is the end of lecture part 1 for neurological disorders I apologize that
it ran over the time limit but I will see you for part 2

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