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Neuro Packets Dementia

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					Neuro Packets- Dementia
Pablo O. Medina

1.a. This patient is exhibiting intentional dementia, most likely of the akinetic type. The frontal lobe is system is the most
predominantly affected area; this system includes frontal lobes, basal ganglia, parts of the thalamus, deep white matter, and dopamine
pathways.

1.b. The differential diagnosis:
akinetic intentional dementia – hypertension, stroke, neuroleptic use (metoclopramide)
kinetic intentional dementia – head trauma, family history, alcoholism
intentional dementia in general –
          hydrocephalus – communicating and obstructive
          neoplasms – frontal lobe, corpus callosum, cingulated, colloid cyst of 3 rd ventricle, primary CNS lymphoma
          vascular – Binswanger’s disease, AComA aneurysm, thalamic infarction, vasculitis
          drugs – neuroleptics
          nutritional – B12 deficiency
          degenerative – progressive supranuclear palsy, Huntington’s dz, Parkinson’s dz, Metachromatic leukodystrophy, thalamic
          degeneration, Pick’s dz, Wilson’s dz, Alzheimer’s (rare), etc. (Huntington’s and Picks or more fronto-temporal dementias
          with inappropriate behavior unlike our pt.)
          infection – AIDS, Creutzfeldt Jakob, Syphilis, Lyme dz, chronic meningitis, PML
          inflammatory – Behcet’s dz, MS, vasculitis
          toxic-metabolic – EtOH dementia, anoxic insults
          trauma
Due to this patient’s longstanding hypertension, as well as multiple CNS acting drugs (Clonidine and metoclopramide) I would further
investigate vascular and drug related causes of dementia. With the history I currently have in the question stem, I would tend to lean a
little more toward the akinetic type.

1.c. I would perform a variety higher cortical function tests to test frontal lobe function including:
 Thurston Word Fluency – pt may produce far fewer words than a normal subject (Normal = dozen or more, frontal lobe dementia = 3-
4). The patient may also produce these words right away and then sit the rest of the minute with minimal effort to try for more.
Contrasting programs – pt may exhibit echopraxia and will mimic the examiner rather than do the opposite as instructed.
Crossed response disinhibition – pt may raise the hand being touched rather than the opposite hand
Constructional praxis (Drawings of a house) – patient may exhibit preservation like many extra and retraced lines.
Praxis – pt may exhibit utilization behavior, such as using a pen as a comb


1.d. Neuro exam findings:
Intentional Dementia (in general) – Patients may exhibit abnormalities in Thurston Word Fluency with pt producing only 3-4 words
right away and then sitting the rest of the minute with minimal effort to try for more. Abnormalities in Contrasting programs and
Crossed response disinhibition may be noted with the patient exhibiting echopraxia and raising the hand being touched rather than the
opposite hand, respectively. In Constructional praxis (Drawings of a house) the patient may exhibit preservation like many extra and
retraced lines. Frontal lobe release signs may be noted although they are not sensitive or specific. Visual grasp signs may also be
noted although it can also be present to cognitive dementia. The patient with intentional dementia may also exhibit urinary
incontinence and gait apraxia with a wide based, unsteady gait with a shortened stride. The patient may also have difficulty making
turns when trying to sit down and have marked impairment of the lower extremities. The patient should have no abnormalities in
cranial nerve function. In pt’s with intentional dementia caused by Binswanger’s disease the examiner my find that the patient has
impairment in declarative memory acquisition.

1.e. CT scan can be used as a diagnostic test and may sometimes come out normal; if abnormalities are noted, the CT scan will usually
show some ventricular enlargement, periventricular reduction, and several discrete lacunae. Abnormalities diagnosed on MRI scan
with T2, FLAIR, and proton density are extensive areas of increased signal in the deep hemispheric white matter, which may help
distinguish MS, leukodystophies, or Binswangers). Other diagnostic tests that can be use to discover the etiology of intentional
dementia include TSH/T4, CMP with Mg, Ca, and Phosphate, ESR, B12, VDRL, HIV test, and urine toxicology screens. Lumbar
punctures may also be of value in ruling out certain causes as may a trial of removal of any CNS acting drugs that a patient may be
taking.

1.f. The top two things in my differential diagnosis of this patient would be medication induced intentional dementia and intentional
dementia caused by Binswanger’s disease. Binswanger’s disease is the most common cause of intentional dementia, and due to this
patient’s long standing hypertension, he is at risk Binswanger’s disease presents as the akinetic form of intentional dementia which is
consistent with our patient, and the underlying mechanism involves demyelenative lesions throughout the brain secondary to lacunar
infarctions. However, due to our patient’s rather quick onset of dysfunction as well as it’s relatedness to recent medication changes
that can cause dementia, the most likely diagnosis is dementia that is medication induced. The patient’s newest medication is
Metoclopromide which can interfere with dopamine receptors in the brain and is considered a neuroleptic. Neuroleptics can produce
frontal system impairment because of their effect on dopamine receptors and can produce tardive dyskinesia, extrapyramidal
symptoms, anxiety, and sedation. The pt was also put on Triavil one year ago, which is a combination of a tricyclic and a tranquilizer
and is also considered to have neuroleptic and anticholinergic properties with the same side effects. Perphenazine, the tranquilizer
component, is a dopamine D1D2 antagonist. Although this med is unlikely to have caused the acute decline in mental function alone,
because he has been on it for a year, it could contribute because of the addition of another neuroleptic. Clonidine, antihypertensive, is
also a CNS active drug by acting centrally on alpha2 receptors and possibly causing CNS depression. Clonidine may have a reaction
with TCAs causing a problem for this pt as it may increase the effect. Thus it was likely the addition of metoclopramide to this highly
CNS depressant medication regimen that caused the acute decline. Accordingly, neuroleptics have been shown to decrease brain
neuroplasticity, which could also contribute to his decline.

2.a. This patient’s dementia is mostly likely due to the form of dementia called attentional dementia, also known as delirium or an
acute confusional state. The hallmark of attentional dementia is a decline in attention or arousal, which is not characteristic of chronic
dementias. Although this patient has a 3 year history of Alzheimer’s disease, his acute decline and behavioral features are not
characteristic of AD. AD is termed a cognitive dementia and characteristically affects the entire cerebral cortex, most often the
parietal and temporal regions. In attentional dementia the midbrain RAS is what is affected. In AD, there is a slow cognitive decline
and personality is usually preserved and language disorders are characteristic, which is not present in this gentleman. Also, patient’s
with AD usually present with findings of agraphia, apraxia, anomia, aphasia, and marked difficulty performing activities of daily
living. This patient exhibits classic symptoms of attentional dementia, or an acute confusional state. His symptoms of falling asleep
during the exam and delusions worse at night (sundowning) are typical of attentional dementia, not AD.

2.b. In this patient’s 1-month history of decline, it is the midbrain reticular activating system and thalamus that are likely involved.

2.c. The differential diagnosis of attentional dementia includes toxic and metabolic disorders, CNS and systemic infections (UTI’s),
and structural processes, such as tumor or a subdural hematoma. Drugs can also cause attentional dementias and common ones are
diuretics or CNS acting drugs, which our patient is on HCTZ. More specifically the ddx includes:
drugs – anesthetics, EtOH, barbituates, opiates, anticholinergics, benzo’s, TCAs, neuroleptics, diuretics
metabolic disorders – hepatic, renal, electrolyte, glucose, thyroid dz, hypoxia, vit deficiencies, hypercapnia
infections – meningitis, encephalitis, AIDS, sepsis, UTI, prostatits, pneumonia
neoplasms – meningeal carcinomatosis, disseminated cerebral mets
herniation syndromes
vascular – infarcts of top of the basilar or midline thalamus, hypertensive encephalopathy, hyperviscosity syndrome, vasculitis, TTP,
DIC, anti-PL syndrome
toxic – formaldehyde, lead
sleep disorders – quantitative and qualitative abnormalities, sun downing
acute/subacute head trauma
anoxic damage
immune-mediated – SLE, para-infectious, sarcoidosis
epilepsy – partial complex status epilepticus

2.d. There are many elements in the patient’s history accounting for his attentional dementia symptoms. First off, he is unsteady on
his feet and falls a lot which can predispose him to subdural hematoma, which are more common in the elderly due to the overall
shrinkage of the cerebral cortex. Falls or hematoma could also cause a type of herniation syndrome that can be associated with his
symptoms. The patient’s medications may be a significant contributing factor. He is taking Donnatal elixir which contains
phenobarbitol, atropine, scopolamine, and alcohol, each of which can cause neurologic disturbances. Also, he is taking HCTZ, which
is a medication that can cause metabolic disturbances as well as causing the dementia. The patient’s low-grade fever and diaphoresis
could be a sign of a possible neurological or systemic infection leading to the dementia symptoms as well. The positive Babinski
signs bilaterally are indicative of an upper motor neuron disturbance, which could signal a structurally related cause to his dementia.
Lastly, his history of an underlying degenerative dementia is also considered a risk factor for attentional dementia.

2.e. For this patient, diagnostic tests in the work up should include a CBC with differential, ESR, CMP with Mg,Ca,PO4, T4 and TSH,
and B12. A urinalysis is useful to diagnose UTI, discontinue any CNS acting medications, and thiamine administration could be
helpful. As for tests to be performed on the day of presentation, a CT scan may also be of use since hematoma is suspected. Later
tests might include MRI, EEG, CXR, ABG’s, blood cultures or lumbar puncture, or an empiric trial of antibiotics.

2.f. This patient’s prognosis is relatively good if the underlying etiology and can be determined and efficiently treated. Most causes of
attentional dementia are treatable, however, they are likely to be fatal if left untreated. For this reason, all patients should be evaluated
extensively. The attentional symptoms should resolve after treatment, however, this patient will most likely continue to experience a
cognitive decline due to his prior diagnosis of AD.

3.a. This patient is exhibiting signs of early Alzheimer’s Disease with amnestic dementia. The neural systems that are most likely to
be involved are the cerebral cortices, most like the associated cortex bilaterally, particularly in the temporal and parietal regions. This
patient is exhibiting a characteristic language disorder called anomic aphasia with word finding difficulty, which results from damage
in the dominant hemisphere. Her difficulties with visual-spatial skills and reproducing simple drawings results from deficits in her
non-dominant hemisphere. The patient’s personality has remained intact which is characteristic of AD. The reticular activating
system and dopaminergic pathways seem to be spared. This patient’s disease is not advanced as she does not yet exhibit significant
apraxia that she is not yet having difficulty with her ADL’s.

3.b. As mentioned above this patient exhibits anomic aphasia in which she can generate fluent output that is devoid of content and has
little meaning. She has significant difficulty with word finding. She also has trouble reproducing simple drawings, and is frustrated
and apologetic about it. All of the above are characteristic of early AD. This patient was also brought in by her family with
complaints that she is forgetting things and tends to repeat herself. This is characteristic of anmnestic dementia, although the patient is
not in denial about this. She displays both recent and remote memory loss.

3.c. The clinical features most inconsistent with the diagnosis of AD is that she does not yet have impairment in her ADL’s. Another
inconsistency is that most patients are oblivious and in denial about their impairments, whereas this patient seems to be knowledgeable
about her deficits. These types of patients are often suffering from a functional amnestic dementia or psuedodementia, which is
caused by depression. Another uncharacteristic feature of her presentation is the quick timing of 3 months onset since most AD
progresses slowly over years.

3.d. Other important questions to ask when evaluating patients presenting with memory loss include to find out if the patient has
experienced any recent or past head trauma, had a past history of cancer, had a history of vascular disease, or had a history of fever.
Sleep disorders should also be evaluated for. Another important and treatable cause of memory loss or dementia like symptoms is
depression. As with most CNS disorders, careful review of the patient’s medications is important as well as drug or alcohol use.
Family history of AD would also be useful knowledge.

3.e. Other abnormalities which could be found on examination are acalculia, alexia, agraphia, agraphesthesia, and right-left confusion.
Another abnormality could be inability to recall 3 objects and a low score of the MMSE.

3.f. When AD is suspected an MRI of the brain is the standard of care. Other diagnostic studies include VDRL, B12, TSH, or a CT
scan. Since this patient is a little atypical in her presentation due to the inconsistencies listed above, a more extensive workup could
be warranted.

3.g. In this patient, the physician should advise the pt and the family about the diagnosis of early AD. It would be important to make
sure that the family understands that this is a progressively declining illness with no cure. Current therapy is based on symptomatic
relief and lifestyle modifications, although there are some cholinesterase inhibitors that may be effective is slowing the progression of
disease, especially in this patient since she seems to be early in the course. They should also be counseled regarding proper sleep and
CNS active drugs. Instruct the pt and family to watch out for any rapid declines or change in attention or arousal, as they will need to
be worked up emergently. They should be encouraged to start discussions on Advance Directives, wills, and choice of a surrogate
decision maker. Also to discuss long-term care, including nursing home placement. Another topic that should be discussed includes
caregiver burden and resources to help the family cope with the impending changes in the family unit.

3.h. Current therapy for AD includes a class of drugs called cholinesterase inhibitors (Aricept) which may slow the progress of disease
in some individuals. These drugs can also help improve adverse symptoms the patient is experiencing. Education and a neurology
consult could be helpful. Treatment for depression using an SSRI and sleep disorders could be beneficial if the underlying mechanism
turns out not to be AD.




Neuro Packets- Epilepsy
Pablo O. Medina

1.a. This patient is most likely experiencing primary generalized epileptic seizures, i.e. grand mal seizures. These type of seizures are
characterized by loss of consciousness, falls, tonic clonic posture and activity, cessation of respiration, incontinence and are followed
by a post-ictal period, each of which are characteristic for this patient. This patient is most likely not having functional spells, as these
spells are usually triggered by some sort of stressor or distressing event. To gather further information, I would ask the patient to take
me back to the onset of his seizures five years ago, and would like further details about his seizure episodes. For instance, how long
the seizure spells last and a more detailed recollection of the exact movements during the seizure would be useful information for
confirming the type of seizure. Also, knowing more details of the patient’s accident at age 10 may be helpful as loss of consciousness
of greater than 30 minutes can cause posttraumatic epilepsy. I would also want to know a more detailed history of his medication use,
such as when the patient was first started on Dilantin, what was his starting dose and was it ever effective in reducing the frequency of
his seizures or if it made his seizures worse, which can be the case with functional seizures. I would also want to know if there were
any big changes in his life or with his medications in the last couple of months that could cause the seizure frequency to increase.

1.b. The differential diagnosis for this patient’s epilepsy is primary epilepsy or secondary epilepsy. Chronic seizures, which is the
case with our patient, are most commonly caused by trauma, neoplasia, phakomatoses, neuronal migration disorders, and mesial
temporal sclerosis, migraine, or worsening of multiple sclerosis. Acute seizures can be caused by metabolic disorders, drug or alcohol
withdrawal, encephalitis, acute stroke, or syncope. Trauma would be the most likely diagnosis in this patient; however, the fact that
he developed his first seizure ten years after the trauma is uncharacteristic because the chance of developing epilepsy greatly declines
2 years following the trauma, although he is at a slightly increased risk than the general population.

1.c. A detailed history plays the largest role in the diagnosis of epilepsy. The most important part of the neurological exam in this
patient would be engaging in actions that would help identify whether focal deficits were present. This would include evaluating for
memory or language impairments, along with praxis, visual-spatial, and motor and sensory abnormalities. If there is a specific lesion,
these can help to localize the lesion to a specific hemisphere. Cranial nerve exams would be important for this reason as well. Also,
upper motor neuron signs such as spasticity and Babinski responses could be helpful. Since this patient is on Dilantin therapy for the
past five years, it would be important to assess for signs of toxicity such as lethargy, imbalance, anorexia, incoordination, diplopia,
and sustained nystagmus. Long term affects of dilantin are osteoporosis, gingival hyperplasia, and hirsuitism.

1.d. Diagnostic studies that would be useful in this patient would be an EEG, serum dilantin levels, serum electrolytes, metabolic
profile, MRI, and lumbar puncture. EEG is very useful in distinguishing primary from secondary epilepsy, as primary epilepsies
usually exhibit characteristic EEG findings. The other listed studies can help rule in or out disorders in the differential listed in
question B.
1.e. Phenobarbitol is an older AED and is not often used in the treatment of epilepsy because it has significant side effects, which
include sedation and causing seizures. It also requires blood level monitoring and the potential for drug dependency exists, abrupt
cessation may precipitate withdrawal, including status epilepticus in epileptic patients. A better alternative would include some of the
newer AED’s and consider a drug with the most convenient dosing schedule, reasonable cost, and least adverse and life altering side
effects. Some of these include gabapentin, lamotrigine, topiramate, levetiracetam, oxcarbazepine, zonisamide. To determine the
optimal anticonvulant dosage one should carefully titrate the does to efficacy (which is seizure free), while monitoring closely for
signs of toxicity (which are listed in question C) and for maximal seizure control.

1.f. The automobile accident is significant in this patient because trauma is the most common cause of secondary epilepsy. The
proposed mechanism is that hemorrhage into the brain leads to the release of free iron, which can generate free radicals and damage
neuronal membranes causing an epileptic focus. The incidence is most common when there is loss of consciousness greater than 30
minutes and during the time most immediately following the trauma. Trauma is questionable as the etiology in this patient as it has
been 10 years since his accident and the development of seizures most commonly occurs during the first 2 years.

2.a. The potential causes of this gentleman’s acute seizure are an acquired metabolic disorder (hypomagnesia, hypocalcemia, etc),
drug or alcohol withdrawal, neoplasm, encephalitis or meningoencephalitis, trauma, syncope, or an acute stroke or lacunar TIA. The
above are causes of secondary stroke. Primary stroke is unlikely in this patient due to his late age of onset. The most likely cause is
hyponatremia secondary to HCTZ therapy.

2.b. Diagnostic studies should include EEG, serum dilantin levels, serum electrolytes, metabolic profile to evaluate electrolytes, MRI
to evaluate for structural causes, and lumbar puncture to evaluate for infection. An EKG could help determine if there was a cardiac
cause of syncope. EEG is very useful in distinguishing primary from secondary epilepsy, as primary epilepsies usually exhibit
characteristic EEG findings.

2.c. This patient should not immediately be put on an anticonvulsant drug. First, the etiology must be confirmed and the underlying
cause of the seizure should be treated if it is treatable. Some circumstances to consider when deciding whether to initiate
anticonvulsant treatment are whether or not the patient drives or works in a hazardous environment. If the patient were to experience
another seizure or was at high risk for recurrent seizures then anticonvulsant treatment would need to be implemented. High risk for
recurrent seizures include a history of brain injury, CT or MRI abnormalities, mental retardation, focal abnormalities on neuro exam,
or a partial seizure as the first seizure. If no cause was discovered the patient should then be cautioned about driving.

3.a. The most important possible causes of this patient’s spells is functional epilepsy, or spells of psychogenic origin (psuedosiezures).
These spells are precipitated by stress or distressing events, oftentimes they follow migraines. Another potential cause of her spells are
a partial seizures, which are highly variable in their presentations and caused from a specific seizure focus. The seizures may also be
induced by her medications.

3.b. In order to discriminate between a functional spell and a grand mal spell a detailed history of the patient’s behavior during these
spells is warranted. Grand mal spells are often violent, have arm movements that are asynchronous from side to side, and may take
place in unlikely positions. They are also followed by post-ictal periods. Functional spells often last longer than grand mal seizures
which only last 1 to 3 minutes. The patient’s lack of response to anticonvulsants is significant in making the diagnosis, as
anticonvulsants are often known to make functional spells worse. We do not have much information on the patient’s overall general
health; however, she could have emotional issues or anxiety since she is treated with clonazapam which can contribute to
psuedoseizures.

3.c. The importance of a normal EEG allows it to shift the suspicion to a more benign cause. EEG’s only have modest sensitivity and
specificity and is not used to rule in or rule out epilepsy, however, it can be used in conjunction with the patient’s history to shift the
pretest probability toward or away from a diagnosis of epilepsy. A negative or normal test as was found in this patient does not rule
out epilepsy, however, it does decrease our suspicion of true epilepsy. EEG’s are also helpful in determining the type of seizure
whether it be of primary, secondary, or absence origin.

3.d. Since this patient’s medications appear to be of no benefit and may in fact be worsening her symptoms they should be gradually
tapered off and eventually discontinued. If her symptoms worsen, this could signal partial seizures as the etiology. This should be
done one at a time, and with close monitoring of her symptoms. Also this patient will have to abstain from driving since discontinuing
anticonvulsants requires patients to give up driving for a substantial period of time even if they are living a normal active life.

3.e. If the patient were found to have psychogenic triggers, treatment of underlying anxiety or depression can successfully be treated.
A psychiatry consult may be warranted in this patient. If it is later determined that the seizures are partial seizures caused by a focus,
trial of a new or different anticonvulsant. Surgical resection is a last resort treatment.

4.a. The differential diagnosis for this patient is absence seizures, hearing impairment, psychosocial problems, physical or sexual
abuse, partial seizures, or functional seizures. Absence seizures are classic in childhood and are usually benign and resolve by adult
hood in the majority of patients. They also can manifest themselves, as a decline is school performance. They are characterized by
blinking, staring, or small automatisims. Additional history I would want is whether or not the girl is aware of any distinct episodes of
staring or spaciness, how long the episodes last, if she feels any confusion after the episodes, or if she remembers the episodes. I
would like to interview her family and/or friends to get a detailed account of the episodes. I would also want to know a detailed
obstetric history of her mother such as if she smoked or used drugs during her pregnancy, as well as if there were any anoxic injury,
brain injury, or complications during her birth. I would also like to know her childhood history of any major trauma or illnesses, as
well as a history of her developmental milestones. All of the above could help explain the etiology of her staring spells.

4.b. I would order an EEG first off, as absence seizures usually have a signature eeg finding and is a major component in making the
diagnosis. In addition a BMP could evaluate for metabolic causes and a hearing exam could help rule out hearing impairment as a
cause for school decline. Other helpful tests may be IQ or achievement testing as well.

4.c. If this patient were diagnosed with epilepsy causing absence seizures ethosuximide would be the treatment of choice. If this did
not work for the patient, another treatment is Valproate. The treatment will depend on this patient’s tolerability of the medications as
well as the varying side effects of each.

5.a. This patient’s level of seizure control is of concern because he is having 3-4 seizures/ year. Efficacy of treatment is to be seizure
free, even less than 1 seizure per year. Therefore, this patient is not being effectively controlled on Dilantin. Although his serum
levels are in the therapeutic range, the levels that can help provide significant relief are highly variable between individual patients.
Hepatic and renal failure can alter the therapeutic range of dilantin, and due to individual variability in drug kinetics, one patient may
exhibit toxicity at 10mcg, whereas another may do perfectly well on levels in the 25-30 mcg range. To determine whether a patient is
in his or her own therapeutic range, saccadic breakdown of ocular smooth pursuit can be examined for, and it is not present in this
patient.

5.b. Since the patient is not experiencing a decrease in the frequency of his seizures, or experiencing any toxic effects from dilantin,
his dose can be carefully and slowly titrated upwards until an efficacious dose is reached. It must be kept in mind that at high doses
dilantin has zero-order kinetics which can make the titration process difficult. His current physical exam tells us that he is not in his
therapeutic range because he has not experienced breakdown of ocular smooth pursuit. One could gradually increase the dose by 25-
50mcg/ml as the maximum dose is 1000 mg/day, and carefully monitor for signs of toxicity. If efficacy could not be reached on this
drug alone, you could consider adding a second agent to help achieve a seizure free state.

5.c. Ranitidine should be used to treat a GI disorder in this patient rather than cimetidine because cimetidine is a potent P450 inhibitor,
which can greatly increase dilantin levels in the body and cause toxicity.
5.d. If the patient reported a recent increase in seizure frequency despite taking all of his medication, concerns would be raised about
hepatic or renal failure which could cause a new metabolic abnormality. Another issue could be that he has become tolerant to his
current medications or started a new drug that is a P450 inducer and increases the degradation of dilantin. He could have a new cause
of secondary seizures on top of his underlying seizure focus and one could order CBC, LFT, BMP to search for signs of infection,
metabolic, or liver abnormalities. A CT scan or MRI could be done to search for structural causes as well.

5.e. Since this patient has been refractory to medical treatment, complete seizure control may be able to be obtained with surgical
resection of the epileptic focus in the brain.


Neurology Packets- Headache
Pablo O. Medina

1.a. Locations that could cause this patient’s pain are the temporal or carotid artery, the epidural space, the subdural space, any layer
of the meninges, the subarachnoid space, the cortical or parenchymal matter, the lateral ventricle, the cavernous sinus, the orbit, CN5,
CN7, CN8.

1.b. Temporal Arteritis: given the patient’s age (over 60 yo), this must be ruled out. This typically presents as a new onset headache
over the temporal region, which can progressively worsen, and is unilateral. The headaches stereotypical of temporal arteritis are also
continuous and non-fluctuating, without specific aggravating factors, all of which are consistent with this patient’s history. Patients
with temporal arteritis may also experience systemic symptoms, such as malaise, fatigue, fever, generalized muscle aches, and
unexpected weight loss.

Tumor (malignant or benign): which must be heavily considered, given her past history of breast cancer. Other tumors could account
for her headache and additional symptoms, including primary tumors involving CN7 or CN8 (schwannoma), the meninges
(meningioma), or the parenchyma. These etiologies could present as constant progressively worsening headaches not aggravated by
cough or the Valsalva maneuver. Temporal pain could also be due to referred pain from a tumor of the cavernous sinus or floor of the
middle cranial fossa. A tumor of CN5 or CN7 could also cause the patient to have a diminished corneal reflex. Given her history of
radiation exposure, she is also at a higher risk of developing various head and neck cancers.

Subdural Hematoma: often occurs post-trauma (of any degree) and tearing of the bridging veins. Chronic subdural hematomas occur
more often in the elderly due to cerebral atrophy of aging and stretching/weakening of the cerebral veins. This patient’s presentation
of unilateral pain and fatigue would be consistent with chronic subdural hematomas.

Chronic Daily Headache: this patient does not present with tractions symptoms, which are not seen with chronic daily headaches. This
patient reports continuous and disabling headaches, which is typical for this diagnosis. Patients with this headache syndrome can also
meet chronic fatigue syndrome or fibromyalgia criteria, which may account for the patient’s other symptoms.

1.c. Given her past history of breast cancer and radiation exposure and a questionably diminished corneal reflex, an MRI of the head
and neck with and without contrast should be obtained. A CBC, ESR, and CRP should be obtained and a temporal artery biopsy
should be performed if these inflammatory markers are elevated.

1.d. If the MRI revealed multiple intracranial masses, metastatic breast cancer could be clinically diagnosed without a tissue biopsy. If
a single mass is noted, then the diagnosis would not be as “clear-cut” and a biopsy would be worth obtaining to definitely identify the
tumor type and allow for best (if any) treatment. Temporal artery biopsy is the gold standard for diagnosis of temporal arteritis,
however, if there is high clinical suspicion or abrupt vision loss, an empiric trial of high-dose corticosteroids can be done. If the
patient has contraindications to steroid use, then artery biopsy confirmation may be necessary before initiating steroid treatment.

1.e. Temporal Arteritis: High-dose Corticosteroids, which are likely to be effective in relieving symptoms and preventing blindness.
There is a better prognosis with early initiation of treatment.

Tumor: surgery to resect the tumor, chemotherapy, radiation therapy, which is likely to be effective if a tumor is the cause of headache
and fatigue, but these options will be heavily dependent on the location of the tumor(s).

Chronic Subdural Hematomas: Corticosteroids may also be used to reduce any swelling of the brain. However, surgery is often
required to relieve pressure, drain remaining blood, and remove blood clots.

Chronic Daily Headache: Fioricet and Ibuprofen can be used to prevent or lessen headache symptoms, and a short acting opiate can be
added if adequate pain relief is not achieved otherwise. However, this headache syndrome is notorious for being unresponsive to
treatment.
2.a. This patient most likely has headaches characteristic of common migraine headaches. These headaches are associated with little to
no neurologic symptoms before onset, which agrees with this patient’s history. She denies aura, vomiting, photophobia, or
phonophobia, which are symptoms that are more characteristic of classic migraines. She also prefers to lay in the dark when she is
experiencing a headache, which is characteristic of migraines in general. She also has a family history that is positive for migraines.
Additionally, she reports symptoms of the “cortical spreading depression of Leao” that is characteristic of common migraines.

2.b. Additionally, I would want to know if there are certain foods(chocolate, red wine, cheese), scents, or situations that are triggers
for her headaches. I would also want to know a step-by-step account of what she feels or senses prior to the headache onset, as this
may be of help when attempting to implement abortive therapy. I would also want to know the most frequent onset time of day and if
these headaches ever occur during sleep or if they interfere with her sleep. In order to accurately assess the above, I would have the
patient keep a detailed diary of her headaches, focusing on their onset, time and situation, symptoms, and triggers.

2.c. No diagnostic testing is warranted at this point in time, as this patient’s history and symptoms strongly suggest a benign common
migraine headache syndrome. This diagnosis would be strengthened if a trial of anti-migraine medication reduces the frequency
and/or intensity of her symptoms. A benign origin is suggested by the fact that her headache is intermittent, she has a history of
similar headaches, no traction symptoms were present, and she had a normal physical and neurological exam

2.d. Three main therapeutic regimens are used in the treatment of migraines. The most successful type of treatment is called abortive
therapy. This regimen works best with patients that have a well-defined and easily identifiable onset. Abortive therapy involves
initiating a carefully titrated medication regimen as soon as the first sign of a migraine appears, ideally within one minute. This
regimen typically relies on different combinations of Fiorecet, Ibuprofen, Midrin, Cafergot, triptans, short-acting opiates, oxygen, or
intranasal lidocaine. If successful, abortive therapy can eliminate 90% of headaches in 90% of patients. A prophylactic regimen can
be used in patients with increasing disability and/or frequency of headaches. The goal of this regimen is to reduce or eliminate the
migraine frequency through the administration of a daily anti-migraine regimen. This is seldom successful, but the most effective
drugs include a long-acting opiate with short-acting opiates for breakthrough pain. Other drugs used for prophylactic therapy include
methysergide, Beta blockers, TCA’s, CCB’s, anticonvulsants, and lorazapam. Symptomatic treatment is used when abortive therapy
was not able to be initiated, has not been prescribed, or is not adequate. In an ER setting, intramuscular opiates are most often used to
achieve analgesia.

3.a. Chronic meningitis or structural processes involving the brain must be ruled out in this patient. Aspects for the patient’s
headaches that lead me to believe this are The onset, months-long time frame, and the fact that he experiences traction symptoms are
strongly suggestive of these etiologies. He also experiences extra throbbing while running. He also has no focal neurologic symptoms
and he develops headache symptoms only after waking and never at night, which is consistent with a structural process. The fact that
his headaches are pancranial, and without N/V, phonophobia, or photophobia, also strengthen the consideration of a structural process.

3.b. A history of trauma could lead to cerebral or dural hemorrhages that cold cause the structural symptoms above. Also, any history
of malformation, such as Arnold-Chiari Malformation would be consistent with the above. Obtaining an ID history is of great
importance as well. I would want to know if he has a history of AIDS or IV drug abuse to rule out a brain abscess. To rule out chronic
meningitis, I would want to know if he has a history of systemic symptoms or fever, vomiting, confusion, neck/body aches, or a
history of chronic corticosteroid use. Exercise-induced migraine can be ruled out because he has no associated aura, nausea, vomiting,
photophobia, or phonophobia associated with his headaches.

3.c. Given the traction symptoms and HPI, a CT with and without contrast or an MRI should be performed immediately to rule out a
large mass, abscess, or hemorrhage. MRI with gadolinium is more sensitive for chronic basilar meningitis. Lumbar puncture should
only be performed if there is no risk of herniation noted on the imaging studies (no masses or structural processes). A CBC could also
be obtained to evaluate for leukocytosis.
Neurology Packets- Dizziness
Pablo O. Medina

1.a. The two leading etiologies in this case are benign positional vertigo and presyncope. I would also like to know if she experienced
any prodromal symptoms prior to the episode of vertigo, such as vision changes, tinnitus, tunnel vision, or weakness, as this would be
more characteristic of presyncope. I would also want to know if the episodes were associated with any chest pain, shortness of breath,
diaphoresis, or tingling in her extremities, which would likely be indicative of cardiogenic presyncope. I would want specific details of
the timing of the event and what the patient was doing immediately prior to the events. I would also want to know if a dizzy spell has
occurred in any other instance other than when she stands up, and if the patient feels like her dizziness is associated with head
movements, as is common in benign positional vertigo. I would also like to know what medications she is currently taking and if there
have been any recent changes to those meds. Some diseases that could predispose this woman to cardiogenic presyncope include
arrhythmias, outflow tract obstruction, pulmonary valve stenosis, pulmonary hypertension, or pulmonary embolism.

1.b. With benign positional vertigo, physical and neurological exam will most likely be normal, but dizziness can be induced using the
Nylen-Baranay maneuver, which involves the physician flinging the patient back into a supine position and looking for associated
nystagmus or pupil dilatation, and the patient will develop symptomatic dizziness within 1 to 5 seconds. To evaluate for presyncope,
the carotid sinus massage or tilt-test maneuvers can be performed. In the carotid sinus massage test, a patient with positive findings
will have asystole longer than 3 seconds or a decrease in systolic blood pressure of 50mmHg. The tilt-test and orthostatic blood
pressures may be helpful in differentiating neurocardiogenic causes of the patient’s dizziness.

1.c. The most likely diagnosis here, and the most common cause of dizziness in general, is benign positional vertigo. It is likely in this
patient due to her history of brief episodes(lasting less than 1 minute), association with head movements such as standing up, and
associated nausea. This is more likely than presyncope because she has no prodromal symptoms of weakness, visual changes,
auditory changes/tinnitus, or sweating.

1.d. This patient could have a negative response to the provocative maneuvers due to a process called habituation, which occurs due to
desensitization of the semicircular canal(s) during repetitive episodes of dizziness where each episode shortens in duration until
dizziness is no longer present. The pathogenesis of benign positional vertigo includes the accumulation of debris from the inner ear
into the semicircular canal, causing a semicircular “plug” and preventing normal fluid movement, which alters endolymphatic
pressure. This causes the brain to sense a signal indicating spinning movements with mild changes in head position, which deform the
cupula. The Nylen-Baranay maneuver places the patient in a position for maximal provocation of this process. However, after some
time, the patient’s head movements may serve to disperse the debris that composes the plug, thereby alleviating symptoms
temporarily.

1.e. No diagnostic imaging studies or lab tests are warranted for a diagnosis of benign positional vertigo, as it can usually be discerned
from the HPI and positive induction via the Nylen-Barany maneuver. This patient did not endorse cardiac symptoms during these
events, but an EKG and/or echocardiogram would be useful diagnostic tests in a patient who did.

1.f. One of the most effective treatments for benign positional vertigo is the Semont maneuver, which is used to empty the
semicircular canal of plug-forming debris. This maneuver can be performing in the office and taught to the patient so they can repeat it
at home as necessary, often twice daily until symptoms resolve.

2.a. The leading diagnosis in this patient is likely to be multifactorial disequilibrium disorder of the aged. This also happens to be the
most common cause of disequilibrium in the elderly.

2.b. I would also like further history regarding the patient’s medications, including recent ototoxic drug use (antibiotics, furosemide).
I would also like to know if the patient has a history of vision loss, hearing changes, tinnitus, or sudden weakness. I would also like to
know if he has sustained any significant trauma that could be the origin of a subdural hematoma. A history of alcoholism, B12
deficiency, diabetes, vascular disease, or cervical spondylotic myelopathy would also be significant in distinguishing the cause of this
patient’s symptoms.

2.c. In this patient, it is imperative to exam vestibular function, visual function and acuity, cerebellar function, dorsal column function,
and ambulation ability. Testing the VOR and visual acuity will assess vestibular and vision function. Vibration and position sense
should also be tested, as well as postural reflexes, and a Romberg test should be performed. Cerebellar functional can be assessed
with heel-to-shin, finger-to-nose, and dysdiadochokiniesia (rapid alternating hand movement) examination. Strength, tone, and reflex
testing should also be performed in the lower extremities of this patient. Focal neurologic deficits should also be assessed for to rule
in/out the possibility of stroke, tumor, or other lesion.

2.d. Abnormal higher cortical functioning in this patient may be related to ischemic damage secondary to lacunar strokes stemming
from his long history of hypertension. This could manifest as UMN signs on exam, such as hyperreflexia, hypertonicity, or a Babinski
sign. His gait abnormalities could also be secondary to periventricular ischemic demyelination or degeneration of the midline
cerebellum. This could manifest as poor cerebellar function on examination, such as impaired finger-to-nose, heel-to-shin, or rapid
alternating hand movement testing.

2.e. The factor most likely contributing to this patient’s disequilibrium is age. Increased age predisposes this patient to decreased
vision, decreased vestibular acuity, muscular atrophy/weakness, and arthropathies. The long history of hypertension in this patient
may also be a significant contributor, as it predisposes him to ischemic damage in the CNS.

2.f. An MRI or a CT scan to look for structural or neurodegenerative causes should be obtained. A polyneuropathy work-up in this
patient should include evaluating B12 levels and fasting glucose and/or Hb A1c for suspicion of diabetes mellitus.

2.g. First priority is to correct underlying disorders/conditions that may be contributing to the disequilibrium, including B12
deficiency, hypertension, or diabetes. Visual acuity impairments must also be corrected. Many patients benefit from ambulation
assistance, such as a cane or rolling walker, and strength, ambulation, and balance training from OT/PT is useful as well.

3.a. The two most likely etiologies of this patient’s dizziness are benign recurrent vestibulopathy (Meniere’s disease) and migraine-
associated dizziness. I would like to know if the patient’s dizziness is associated with headache, visual or sensory symptoms,
parasthesias, photophobia, or phonophobia, as this would be more suggestive of migraine-associated dizziness. I would also like to
know if she has experienced and tinnitus or hearing loss, or if she has a history of hypertension, as this would be more suggestive of
benign recurrent vestibulopathy. A more thorough history of the “dizziness” must also be obtained, including frequency and time of
occurrence, associated activities, and known precipitants. Of high importance is whether the dizziness is present while motionless or if
it is only present with movement of the head.

3.b. No specific diagnostic studies are warranted in this patient. However, a thorough physical exam should be performed to assess for
focal neurologic symptoms. If present, a CT or MRI may be needed to evaluate the cause of these impairments.

3.c Migraine-associated dizziness should be treated with prophylactic and/or abortive migraine therapy. Abortive therapy includes
using such medications as Fioricet, ergot derivatives, triptans, and short-acting opiates at immediate migraine onset. Prophylactic
therapy with anticonvulsants, beta-blockers, CCB’s, TCA’s, NSAIDs, or long-acting opiates may be useful if abortive therapy fails to
prevent the dizziness. Treatment for benign recurrent vestibulopathy includes scopolamine patches or meclizine, which would also
alleviate the associated nausea in this patient. Other medication options include carbonic anhydrase inhibitors or loop diuretics. As a
final resort, labyrinth obliteration may be performed, but the patient will be deaf in that ear and the contralateral labyrinth may be
affected in the future.

4.a. This patient’s history is most suggestive of presyncope with associated syncopal episodes. The stiffening and jerking experienced
by the patient most likely signifies a post-ischemic seizure, as this is common in syncope patients. Epilepsy can be ruled out as true
epileptic seizures rarely have preceding dizziness.

4.b. A more thorough history needs to be obtained, including assessment for other pertinent symptoms of presyncope, such as tinnitus,
shortness of breath, air hunger, diaphoresis, chest pain, nausea or parasthesias. The history should focus on symptoms to help
distinguish whether the patient’s presyncopal symptoms are cardiogenic or situational. A history of cardiovascular problems, such as
arrhythmias, cardiac disease, outflow obstruction, cardiomyopathy, pulmonic stenosis, pulmonary hypertension or thrombo-embolic
events may be suggestive of cardiogenic syncope. Past and/or follow-up EKGs, echocardiograms, or holter moniter results may be
helpful. To evaluate for situational presycnope, I would like to know if the patient’s symptoms are associated with micturation,
defication, coughing, smoking, orthostatic or positional changes, or certain emotional situations. Medications such as
antihypertensives, diuretics, and TCA’s can also be iatrogenic causes of dizziness/presyncope.

4.c. The most pertinent aspects of the physical exam would include cardiac, pulmonary, and neurological examination, in addition to
vitals and orthostatic measurements. Cardiac exam should assess for arrhythmias, bruits, murmurs, and pulses. Pulmonary exam
should include pulmonary ascultation for evidence of pulmonary hypertension. Neurologic exam should assess for focal deficits.

4.d. An EKG, 24-hour holter monitor, and echocardiogram should be obtained to evaluate for cardiogenic causes of the dizziness.
Electrophysiologic studies could also be performed if the previous results do not clearly define a cardiac origin. Carotid sinus massage
testing can be used to evaluate for carotid sinus syndrome. Tilt-table testing could be useful in assessing for a neurocardiogenic
etiology. Imaging studies (CT or MRI) should only be ordered if a neurologic cause is suspected.

4.e. If the patient’s presyncope and syncopal episodes is cardiac in nature, then the underlying disease should be treated according to
the protocol for that particular disease. Anticholinergics or sympathetic agonists with propranolol can be used in carotid sinus
syndrome. Neurogenic syncope can be treated with BBs, anticholinergics, theophylline, fudrocortisone, or AV pacing. To treat
orthostatic causes of presyncope/syncope, the patient should be educated to take their time when moving from a lying to standing
position. They should also be informed to stay well hydrated. Situational syncope can be treated by avoiding the stimulus or
understanding alerting symptoms to prevent progression to full syncope.
Neuro Packets- Neuromuscular Disease
Pablo O. Medina

1.a. The most likely diagnosis in this patient is a mononeuropathy due to compression of the median nerve as it passes through the
carpal tunnel (carpal tunnel syndrome). Symptoms of carpal tunnel syndrome can be instigated by prolonged flexion or extension of
the wrist, which is a common position when driving. During pregnancy, fluid accumulates in the carpal tunnel and CTS becomes a
common complaint. Carpal tunnel entrapment involves parasthesias in the median distribution, most commonly affecting the first 3 or
4 digits and lateral hand. It also involves pain in the palm, wrist, forearm, and sometimes arm and shoulder. Physical exam signs to
look for in this patient would be median sensory loss, weakness of thumb opposition, thenar atrophy, and possibly a Tinel’s and/or
Phalen’s sign. Other alternative diagnoses to consider would be ulnar neuropathy, a polyneuropathy, multiple mononeuropathy, a
radiculopathy, a polyradiculopathy, or a brachial plexopathy. Ulnar neuropathy would have weakness and wasting of the intrinsic
muscles of the hand and parasthesias of the 4th and 5th digits, usually due to ulnar nerve compression as it passes through the cubital
tunnel. A multiple mononeuropathy would have an acute onset of sharp pain and development of focal numbness and weakness.
Multiple mononeuropathies are commonly found in areas where nerve compression is uncommon, and this finding usually suggests a
systemic vasculitis. Polyneuropathies more commonly affect the long nerves first and are associated with metabolic or toxic disorders.
Symptoms typically start distally and progress proximally in the characteristic stocking/glove distribution. Patients may experience
tingling or burning sensations, decreased light touch and pinprick sensation, loss of vibratory sensation, muscular atrophy of the feet,
and decreased ankle reflexes. A radiculopathy would present with pain radiating from the neck to the arm, especially during
movement of the neck and/or arm. Sensory deficits caused by a radiculopathy would be confined to that nerve root’s distribution.
Polyradiculopathy presents with weakness that is just as likely to be proximal as distal and sensory deficits do not conform to single
nerves. Brachial plexopathy usually presents with pain and weakness confined to one entire extremity.

1.b. As discussed above, pregnancy predisposes a woman to fluid accumulation within the carpal tunnel, which leads to compression
of the median nerve. Other predisposing conditions for median nerve entrapment are rheumatoid arthritis, myxedema secondary to
Grave’s disease, and acromegaly. Repetitive movements (chronic trauma) or acute trauma can also be a cause of this patient’s
symptoms. Certain conditions, such as diabetes mellitus, Vitamin B12 deficiency, or sarcoidosis, can lead to a mononeuropathy that
could mimic CTS.

1.c. Tinel’s test and Phalen’s test are two commonly-used tools that can help a physician in diagnosing CTS. Tinel’s test elicits pain
and/or parasthesias in the hand(s) when the median nerve in the wrist is tapped just proximal to where it enters the carpal tunnel.
Phalen’s test elicits these same symptoms when dorsal surfaces of the hands are pressed together in prolonged flexion. Light touch
sensation should also be assessed for in the distribution of the median nerve.

1.d. If a diagnosis cannot be definitively made by history and PE, electrophysiologic studies can be used to determine if conduction
abnormalities are present. Nerve conduction studies can be used to determine if entrapment is present and if so, how severe the nerve
damage is. If metabolic abnormalities/toxicity is suspected, then labs should be performed to evaluate.
1.e. Therapeutic options for carpal tunnel syndrome include wrist immobilization, avoidance of instigating activities, and rest.
Lidocaine and steroid injections can also be administered into the carpal tunnel to relieve inflammation and pain. As a last resort,
decompression via release of the flexor retinaculum can be performed.

2.a. Spinal cord lesions often present with little to no atrophy, increased tone, sluggish initiation of movements, posturing, brisk
reflexes, Babinski signs, and central patterns of sensory loss. These lesions could also show segmental signs at the level of the lesion
and autonomic dysfunction such as bowel or bladder incontinence. Radicular disease often presents with radiating pain from the
lower back down into the leg that is precipitated by movement. Pain is found in a radicular distribution and sensory loss is confined to
a dermatomal distribution. Autonomic dysfunction is not present with radicular lesions. Peripheral nerve lesions present with distal
lower extremity numbness, decreased deep tendon reflexes, down-going toes, muscle atrophy and fasciculations, and sensory loss.
Like radicular lesions, automonic dysfunction is not common with peripheral nerve lesions either.

2.b. This patient’s symptoms are most likely due to a metabolic/toxic polyneuropathy. This patient’s symptoms are characteristic of
this deficit: symptoms initially in the feet that progress proximally up the legs and eventually affecting the hands and arms last. Other
polyneuropathy symptoms present in our patient include tingling/burning sensations and loss of vibration sensation in the toes, atrophy
of the intrinsic foot muscles, and reduced or absent ankle jerk reflexes, all of which are present in our patient. Sensory loss in a
stocking/glove pattern is also common in these patients.

2.c. This patient’s ED is likely associated with the same disorder that is causing his peripheral nerve symptoms. Diabetics with
peripheral vascular disease and polyneuropathy often present with ED, as erections are achieved and maintained via the
parasympathetic nervous system. Other signs/symptoms of autonomic dysfunction include incontinence, GI dysmotility,
gastroparesis, and orthostatic changes.

2.d. The differential diagnosis in this patient includes diabetic or uremic polyneuropathy (secondary to endocrine or liver dysfunction),
toxic or drug-related polyneuropathy (from alcohol, heavy metals, NO, or organophosphate poisoning), nutritional deficiencies (B12,
folate, thiamine, or B6 deficiency) and inherited or autoimmune causes (CVDs or Charcot-marie-tooth disease). The diagnostic work-
up should include a CBC to look for anemias, B12 and folate deficiency, ESR and CRP, TSH, SPE, and CMP to look for metabolic
abnormalities such as uremia. An OGTT should be performed and a HbA1c should be obtained to assess for diabetes, and a review of
alcohol, drugs, and medication use should be done.

3.a. This patient’s most likely diagnosis is Guillain-Barre Syndrome, which is a type of autoimmune polyradiculoneuropathy. It is
preceded by infection or stressors in over half of all cases, and some causes such as Campylobacter, CMV, and EBV have been
identified. As in our patient, GBS is characterized by rapid development of generalized weakness, loss of DTRs, and minor sensory
loss. The differential diagnosis includes the Miller-Fisher variant of GBS in which there is prominent sensory loss, chronic
inflammatory demyelinating polyradiculoneuropathy, which is a chronic form of GBS, multiple myeloma, Waldenstrom’s macro-
globulinemia or other benign monoclonal gammopathies.

3.b. Due to the rapid development of muscle weakness in GBS, the infirmary physician should have sent the student immediately to
the ER where she could have been seen by neurology. GBS progresses rapidly over just a few days and can be fatal if respiratory
depression or circulatory collapse (shock) develops unexpectedly.

3.c. During the patient’s hospital stay, her respiratory function should be monitored closely as respiratory failure secondary to muscle
weakness can occur rapidly and unexpectedly. Vital signs, ABGs, and PFT’s can all be used to monitor respiratory function, and if it
deteriorates, intubation can be performed. Patients with autonomic instability can be monitored in the ICU.

3.d. Treatment for GBS most commonly consists of supportive treatment for up to 4 weeks to prevent the possibly fatal consequences
mentioned above. IVIG or plasma exchange can be of some benefit in severe cases.

4.a. If considered individually, most of the patient’s symptoms can be localized to a specific nerve. The patient’s symptoms in the
anterior compartment of his left leg consisting of pain, numbness, foot-drop, atrophy, and weakness of dorsiflexion and eversion are
evidence of peroneal neuropathy. The patient’s weakness and pain in the lateral 3 fingers and thumb, numbness of the palmar surface
of the thumb, middle, and index finger, and weakness of the thenar muscles are all consistent with median neuropathy. The patient’s
numbness in the medial 2 fingers, weakness of finger spreading, thumb adduction, flexion of the pinky and ring fingers, and wrist
extension are suggestive of ulnar neuropathy. The sequential development of these neuropathies is suggestive of multiple
mononeuropathy, which is most commonly due to a systemic vasculitis.

4.b. Carpal tunnel syndrome is unlikely to be causing the RUE symptoms because it is a gradual process most commonly due to
overuse (chronic trauma) and is often instigated by prolonged wrist flexion or extension. This usually occurs over the course of many
years, unlike the acute presentation in our patient. Also, this patient presents with a left ulnar neuropathy which further suggests the
diagnosis of multiple mononeuropathy.

4.c. The most likely cause of this patient’s neurologic symptoms is a systemic necrotizing vasculitis such as polyartertitis nodosa or
Wegener’s granulomatosis. This usually manifests as a sharp pain which represents infarction of the nerve, followed by focal
weakness and numbness and is of acute onset and in sites not common for compression. Our patient presents with this clinical picture.
These disorders are also auto-immunologic in nature, which coincides with this patients RA history.

4.d. Early recognition and initiation is key to the treatment of these vasculitides. First-line treatment usually includes high-dose
corticosteroids and/or other immuno-suppressive agents. Early treatment with antiviral agents in hepatitis C-associated vasculitis are
also beneficial.

5.a. This patient’s presentation is most suggestive of an aquired disorder of the muscle fibers themselves, i.e. a myopathy. This patient
exhibits progressive proximal muscle weakness by having difficulty arising from chairs and climbing stairs. He also has normal
sensation and relatively normal reflexes along with normal CNs and mental status. All of this is characteristic of a myopathy. A CNS
lesion would be manifested by little or no atrophy, increased tone, slowness in initiating movements, posturing, brisk reflexes,
Babinski signs, and central patterns of sensory loss. A PNS lesion would present with decreased deep tendon reflexes, down-going
toes, muscle atrophy and fasciculations, and sensory loss, most often in a stocking/glove distribution. Lesions of the neuromuscular
junction often exhibit muscle weakness without sensory or autonomic deficits. These lesions also impair proximal extremity and
extraocular muscle groups.

5.b. DDx for this patient includes acquired disorders of muscles such as polymyositis, dermatomyositis, sarcoidosis, viral trichinosis,
HIV-related myositis, and drug-induced myositis. Also causing these disorders could be hyper- or hypothyroidism, acromegaly, and
parathyroid disorders. Inherited myopathies should also be on the differential, however, they are unlikely as they usually manifest
themselves in the childhood or teenage years.

5.c. Lab studies useful for diagnosis would include a serum CK, TSH, T4, CBC, ESR, cortisol levels, and an HIV test.

5.d. Nerve conduction studies and EMG studies would definitely be of use in diagnosing this patient. Both Polymyositis and
dermatomyositis have abnormal EMG findings. In distinguishing the locations pointed out in question 5a, nerve conduction studies
will be normal with myelopathies and CNS lesions, and abnormal with GBS. In disorders with PNS involvement, nerve conduction
studies can show some conduction delay. Nerve conduction studies can also be useful in identifying primary demyelinating disorders
and the severity of peripheral nerve entrapment. In disorders of the NMJ, repetitive stimulation and EMG studies can help with
diagnosis. EMGs are useful for identifying specific types of myopathies as well as neurogenic causes of muscle weakness and
denervation causes.

5.e. Two examples of treatable myopathies include endocrine-related and drug-induced myopathies. Hyper- and hypothyroidism can
be treated with thyroid hormone supplements, radio-iodine ablation, thyroidectomy, or other medications and can improve once the
thyroid disorder is under control. Accordingly, drug-induced myopathies can be cured by discontinuing the offending agent.




Neuro Packets- Spine Disease/Myelopathy
Pablo O. Medina

1.a. Other historical information would include more pertinent details concerning the pain, such as what the patient was doing when
the pain began, if it was associated with physical activity, if he has experienced any recent trauma, or if it is provoked by coughing or
straining. I would also want to know if the patient has ever had pain like this before, whether the patient’s occupation or daily
activities could cause repetitive injury, or whether or not the patient has a history of obesity, which could predispose this patient to a
degenerative disease. I would also want to know if the patient has a history of cancer. I would like to know what alleviates and
aggravates the pain, if the patient has tried anything to relieve the pain, and if the patient has bowel/bladder incontinence or gait
disturbances.

1.b. I would suggest the straight leg raise test in which the patient should experience radicular pain. I would also suggest the Lasegue
maneuver, which stresses the sciatic nerve and provokes a radicular pain. If the injury is in the hip joint, pain would not be present
using this maneuver. Another maneuver to distinguish between radicular and hip joint pain is the Patrick’s maneuver which would
elicit pain in the hip joint with a hip joint injury. Accordingly, having the patient stand on their tiptoes and then drop back heavily onto
the heels should elicit pain in a disk herniation injury. A complete neurologic exam should be performed, specifically assessing gait,
reflexes, and a complete musculoskeletal exam of the back and legs. Given this patient’s suspected history of a herniated disk, this
patient should have a positive straight leg test at less than 60 degrees. The patient would also have a negative Patrick’s test, and either
a positive or negative Lasegue depending on whether or not the sciatic nerve root is involved.

1.c. Since the neurologic exam is normal, the most like etiologies of this patient’s symptoms are nerve root or peripheral nerve lesions.

1.d. Since this patient has no neurologic abnormalities on exam, diagnostic studies are not warranted, and a long weekend of bed rest
and conservative therapy should be instituted. In this type of injury, diagnostic imaging studies are usually not warranted until surgery
is being considered an option for treatment.

1.e. For this patient’s treatment, I would first institute complete bed rest for several days, which will allow the herniated fragment to
move back into place. I would also begin an NSAID for its analgesic and anti-inflammatory properties. As time passes the patient
should be instructed to gradually increase activity and participate in exercises to help improve strength in the back and abdominal
musculature. Physical therapy may also be helpful in this patient.

2.a. The etiology of this patient’s presentation is most likely cord compression of the cervical spinal cord at the C6-C7 levels. This is
most likely true because of the decreased DTRs in the biceps, triceps, brachioradialis, and finger flexors. If the lesion were at C5-C6
level, then the patient would have hyperactive triceps and finger jerk reflexes. His lesion is clinically significant due to his iliopsoas
weakness and narrow-based gait. The decreased ankle and plantar reflexes may be explained by a diabetic neuropathy, which can
mask the expected hyper-reflexia below the level of the lesion, and the patient’s history of smoking could lead one to believe that
metastatic cancer to the spine could also be the cause. His symptoms came on quite rapidly over weeks vs. years, which is more
indicative of spinal cord compression than a degenerative process.

2.b. This patient’s bladder function should be tested as his history suggests a spinal cord compression, and not just a nerve root
compression. Cord compression can lead to autonomic dysfunction, which can manifest as acute urinary retention or as chronic
incontinence with urinary urgency. Bladder function can be tested with urinary studies testing different volumes and pressures, and
can be assessed with different maneuvers such as coughing or a Valsalva maneuver.

2.c. The ankle jerk reflexes in this patient may be diminished rather than hyper-reflexic secondary to a peripheral neuropathy due to
the patient’s diabetic status.

2.d. Diagnostic studies for this patient could include a plain AP/lateral spine film, which can detect erosion of a vertebral body or
pedicle. However, MRI is the definitive study because it can define the extent metastasis, which is highly probably given this patient’s
100 pack-year history. We should also obtain a chest x-ray to evaluate for primary lung cancer.

2.e. Suspected spinal metastasis with cord compression should be treated immediately on the day the patient’s disease is first
discovered with both steroids and radiation therapy. One can begin with 100mg of Decadron IV immediately then tapering down to 2
mg PO over the next few weeks. Surgery is only recommended if the patient has spinal instability and the lesion should be biopsied if
the primary is unknown.

2.f. If this patient had a lumbosacral plexopathy due to his diabetes, he would most likely have unilateral deficits and would have
marked limb weakness and atrophy in his iliopsoas and quads. The patient may exhibit femoral nerve deficits with decreased sensation
in the femoral area of the leg and weakness with leg extension. Lastly, the patient may complain of pain in the hip and thigh that is
more severe at nighttime.

3.a. This patient is exhibiting signs and symptoms of degenerative disease of the cervical spine. One important findings from the
neurologic exam that suggest this process is pain beginning in the right side of her posterior neck and radiating down her arm. She
also exhibits difficulty and pain when rotating her head, with an associated sense of grinding or popping, which is characteristic of this
disease process. The tingling down her lateral arm most likely represents a radicular impingement. Also important in the neurologic
exam would be assessment of trapezius and cervical paraspinous tenderness, atrophy or muscle wasting, and depressed DTRs.
Optimal treatment should include medical management with NSAIDS and benzodiazepines. Surgery should be considered if there are
severe neurologic deficits and/or functional impairment, but it may not be successful in relieving pain. Surgery is also recommended if
there are gait problems, spasticity, or spinal instability.

3.b. If the neurologic exam is completely normal, further diagnostic studies are not warranted. Medical management would be
implicated and diagnostic studies would only be of use if surgery were being considered. Conservative treatment for degenerative
cervical spine disease consists of NSAIDS for pain and inflammation, benzodiazepines qHS for muscle spasms, and spine stabilization
with a soft collar.

3.c. EMG/NCVs are not indicated in the patient because this patient’s symptoms clearly exhibit a neurodegenerative disease. These
studies would not alter the course of conservative treatment that we would start with (as described above). If the diagnosis of this
patient was uncertain, these tests could more decisively identify an etiology.

4.a. Given this patient’s case history, he does not appear to have a neurological lesion. If a neurologic(spinal cord) lesion were present
this patient could exhibit symptoms of urinary retention or dysfunction, sensory symptoms, muscle atrophy, spasticity, gait disorder,
abnormal DTRs, or a Babinski sign. Lumbar stenosis or a herniated disk could cause this patient to experience some neurogenic
claudication in the legs, which would be relieved by position change.

4.b. If this patient experienced neurogenic claudication, i.e. radicular-like pain precipitated by prolonged standing, sitting, or walking,
that is relieved within 5 minutes of ceasing of the activity, I would consider the diagnosis of lumbar stenosis, a condition caused by
hypertrophic changes in the spinal canal.

4.c. Diagnostic studies for suspected lumbar stenosis should not be performed until surgery has been decided upon as the treatment of
choice, in which case an MRI would be the study of choice. Also, since lumbar stenosis is caused by hypertrophic changes, the
condition is often not resolved by conservative treatment alone. Although studies are not necessarily warranted in this patient with his
presentation, certain maneuvers such as the Lasegue maneuver and straight leg raise test can be used to clarify the diagnosis. Also,
Waddell signs for symptom magnifiers should be used to clarify the authenticity of this patient’s pain.

4.d. The most likely diagnosis in this patient is chronic low back pain secondary to this gentleman’s aging process and history of back
trauma.

4.e. My treatment plan would consist of encouraging the patient to partake in physical therapy, including back and abdominal
strengthening exercises to help reduce spinal stress and lose weight. Water exercises would also be useful in this patient. Further
treatment would include daily NSAID and muscle relaxant treatment, if needed. Narcotic analgesics should be avoided, if possible, in
this patient.

Neuro Packets- Stroke
Pablo O. Medina

1.a. Considering the fact this patient has intact comprehension and nearly fluent speech with phonemic paraphasias, but poor
repetition, he is exhibiting a conduction aphasia. The lesion can be isolated to the left arcuate fasciculus, which is connects Broca’s
area, the speech center, with Weirncke’s area, the comprehension center. The left arcuate fasciculus is supplied by the MCA, and it
can be localized to the left side for the fact that the patient has right-sided deficits and that the language center is found in the left side
is a majority of individuals. It most likely involves the upper division of the MCA as he has more symptoms in the right arm and face
rather than the lower extremity. Other higher cortical function abnormalities that would appear in a left sided large vessel stroke could
include apraxia, dyscalculia, and heightened emotionality. Gerstmann syndrome and finger agnosia could also be present. He could
also have impaired graphesthesia, impaired optokinetic response, or suppression of background rhythms on EEG. Other signs could
consist of contralateral UMN symptoms such as hype-rreflexia and a positive Babinski sign, along with a contralateral sensory loss,
which our patient presented with.

1.b. The MCA supplies the motor, premotor, and somatosensory cortices of the brain, therefore there are a number of deficits that will
be produced. First, there will be a contralateral homonymous hemianopsia, with deviation of the head and eyes toward the side of the
lesion if the frontal eye fields are involved. Other cranial nerve findings would be weakness of the extraocular muscles (CN 3, 4, 6)
secondary to the eye deviation, decreased sensation in the face (CN5), and lower facial weakness (CN7). Also, an abnormal gag
reflex and tongue protrusion (CN9-12) may be apparent. The major sensory deficit would be loss of sensation on the contralateral side,
other sensory deficits can include impaired position sense and impaired tactile localization. Four motor deficits would include
contralateral hemiplegia and weakness, hypertonicity, spasticity, pronator drift, and hyper-reflexia.

1.c. The EKG shows atrial fibrillation, which is a tachyarrhythmia that can be associated with thromboembolism formation in the
atria, which is a common cause of stroke. This risk can be reduced with chronic anticoagulation or antiplatelet therapy.

1.d. I would obtain a CT scan in this patient if a hemorrhage is suspected, or a diffusion weighted MRI to assess for severity and
localization of stroke. I would also order a CBC, platelet count and ESR to assess for coagulation disorders. A VDRL, HbA1c, and
fasting lipid studies would also be helpful and are commonly ordered in all patients to help guide the diagnosis and treatment of
strokes, as well as to modify risk factors for prevention of a subsequent stroke. An echocardiogram could help assess for a thrombus in
the atrium or septal defects, such as a patent foramen ovale. An ultrasound or an MRA can help assess the patentcy of the carotid
arteries. In select patients, other studies such as fibrin split products, blood cultures, anticardiolipid antibodies, or peripheral smears
can be performed as well.

1.e. As of now we should do nothing about this patient’s blood pressure. During the initial post-stroke days, hypertension should not
be treated unless the pressure is greater than 220/120 in order to maintain the perfusion pressure of the brain and to avoid any further
ischemic damage. The blood pressure should not be reduced to below 190/110.

1.f. Acute treatment for this patient would consist of thrombolytic therapy with rTPA within 3 hours of the onset of symptoms if there
is absolutely no evidence of hemorrhage and the benefits outweigh the risks. Accordingly, one should cardiovert the patient back to
sinus rhythm. Chronic treatment of this patient’s stroke includes preventing another stroke from recurring. This is accomplished by
maintaining sinus rhythm with anti-arrhythmics such as amiodarone or beta-blockers, and chronic anticoagulation if the patient has
underlying heart disease and will be compliant with therapy. Amiodarone is a drug with a lot of interactions and side effects such as
pulmonary fibrosis and hypothyroidism and should be monitored closely if used. Anticoagulation can be accomplished with
Coumadin, with a goal INR range between 2 and 3. Close monitoring of the patient is a necessity as anticoagulation carries significant
risks of hemorrhage. Other chronic treatment is to monitor and treat all risk factors for contributing conditions such as hypertension,
diabetes, and hypercholesterolemia. These patients should be placed on an ACE-I, a statin, and medication to adequately control their
diabetes.

2.a. Due to the absence if aphasia and the fact that the patient is right handed, it is highly unlikely that this patient’s stroke involves the
left cerebral cortex. Also, considering that her stroke presents with pure motor deficits and no sensory deficits, her stroke is most
likely a left-sided lacunar stroke. These strokes are most likely caused by intrinsic microvascular disease and involve the perforating
lenticulostriates.

2.b. The three most common lacunar syndromes involve a stroke with pure motor or pure sensory impairment. Pure sensory
impairment is most likely a lacunar infarction involving the thalamus. Pure motor are localized to the posterior limb of the internal
capsule. Motor impairments involving cerebellar or pyramidal dysfunction and ataxia on the same side of the body usually reflects a
lacunar infarction of the basis pontis, posterior limb of the internal capsule or the corona radiata. The most valuable tool in order to
distinguish between lacunar infarcts and large vessel infarcts is during the initial evaluation of the patient and involves a thorough
higher cortical function exam. Lacunar infarcts are not associated with any evidence of higher cortical dysfunction whereas large
vessel infarcts are. Additionally, lacunar infarcts lack evidence of visual dysfunction in response to an optokinetic stimulus, and also
lack evidence of graphesthesia. Accordingly, large vessel infarcts may present with UMN signs, CN abnormalities, and simultaneous
motor and sensory deficits. Lacunar infarct strokes are more likely to be minor strokes and have a rapid recovery.
2.c. The two possible reasons that this patient’s CT scan could be normal on the third day are 1.) lacunar infarcts may take up to seven
days to become apparent on CT scan, or 2.) due to their low sensitivity, only about 40% of lacunar infarcts are ever detected by CT.

2.d. Other diagnostic studies that would be of use would be a dw-MRI, CBC, platelet count, and ESR, VDRL, an EKG, and also
HbA1c, lipids, and scrutiny for history of ischemic heart disease. Each of the above could help determine the long-term chronic
treatment to minimize stroke recurrence. Since this patient has a significant left bruit, an MRA or Doppler ultrasound studies to assess
the patentcy of the carotids may also be useful.

2.e. Acute treatment for this patient may begin with aspirin, plavix, or aggrenox as various studies have shown that either of these
agents can help reduce subsequent stroke incidence. Depending on how fast the patient recovers from the acute stroke, she should be
monitored closely and rehabilitation may be necessary. Chronic treatment for this patient may consist methods to lessen intrinsic
vascular disease and can be accomplished with an HMG-CoA reductase inhibitors (statins) to lower LDL cholesterol, as well as an
ACE-inhibitor or an ARB, which have also been proven to lower the risk of stroke. Also, chronic aspirin treatment may be beneficial.
Her diabetes should also be closely monitored, as diabetes is also a cause of intrinsic vascular disease.

2.f. This patient should not be considered for a carotid endarterectomy as her stroke is most likely a lacunar infarct, which are almost
always caused by intrinsic vascular disease vs. embolization. Carotid endarterectomies are usually performed in patients with
symptomatic unstable atheromatas that are likely to embolize distally. This procedure strives to remove the source of debris and
emboli. There is also a lot of risk/benefit evaluation when deciding whether to undergo this procedure. This patient does have a left
carotid bruit which could be a source of emboli in the future however, the patient would have to have at least a 70% or greater
blockage in that artery and be symptomatic, and the most success with this procedure occur in patients with 90-99% blockage in their
carotid artery.

3.a. This patient’s lesion can be localized to the left occipital lobe and may include either the left optic tract or radiations based on her
right homonymous hemianopsia, which is evidence of a unilateral infarction. This region is supplied by the left PCA, which branches
from the basilar artery and supplies the posterior cerebrum with circulation.

3.b. The six etiologies that could contribute to this patient’s stroke are:
 1.) A cardiogenic embolism, which may be secondary to a-fib, acute MI, dilated cardiomyopathy, mechanical heart valve, or
infectious endocarditis could be the first etiology. This patient has a mid systolic click, which could be evidence for mitral valve
prolapse or another valvular disease, which could have her at a higher incidence for thrombombolism. A history of drug abuse, recent
dental work, or fevers may be helpful in distinguishing this.
 2.) Collagen vascular disease or vasculitis could also account for her stroke as well as her recent abortions, which could lead us to
explore this mechanism as a cause. She could have a history of SLE with either lupus anticoagulant or anticardiolipin antibodies.
Stroke may also be the initial manifestation of antiphospholipid antibody syndrome.
3.) This patient could have a coagulapathy consisting of a hypercoagulable state, which would predispose her to thromboembolism.
Two disorders that could cause a hypercoaguable state are antiphospholipid antibodies, discussed above, and prothrombin G20210A
polymorphism. Also activated protein C resistance may be associated with increased stroke risk. Again, this patient’s history of
headaches and multiple spontaneous abortions are characteristic of a coagulation disorder. Accordingly, pregnancy in general is
associated with a hypercoagulable state for unknown reasons.
4.) Migraine headaches are also associated with an increased relative risk of stroke (2.8) in patients less than 40 years old. Risk of
stroke is also increased in these patients with migraines if they have other risk factors such as smoking, hypertension, and use of birth
control pills, each of which our patient has. The patient also has a 5-year history of headaches with visual symptoms which could be
signs of migraine with aura and studies have shown that migraine patients in general experience a higher incidence in strokes of all
kinds.
5.) Tumor causing structural compression or a mass effect herniation syndrome could also be a cause of this patient’s stroke. This
could also account for her 5-year history of increasingly worse headaches with visual symptoms, as tumors are usually slow growing
and cause progressively worsening symptoms. This could also result in her vague symptoms of nausea and photophobia.
6.) Seizures of focal origin could also account for this patient’s presentation, as they may be associated with post-ictal syndrome that
can consist of a hemianopsia, which is what our patient is presenting with. Her vague visual symptoms and headaches could also be
her presentation of a seizure.

3.c. In this patient, diagnostic studies should include a CT scan or dw-MRI to assess for tumor, herniation, hemorrhage, or to localize
the area of the lesion. Also, a CBC, platelet count, ESR, and VDRL should be obtained to assess for hypercoaguability, infection, or
vasculitis. An EKG and echocardiogram could be done to assess for atrial fibrillation or structural heart or heart valve abnormalities.
Other labs could be performed to assess for anticardiolipid antibodies, lupus anticoagulant, or ANA antibodies. Other tests for
hypercoaguability can be performed as well, such as factor V leiden or prothrombin mutations. Her other risk factors, such as
hyperlipidemia, hypertension, and diabetes, should be assessed as well.

3.d. Due to having a stroke at such a young age, this patient should be advised to stop smoking, and use a birth control method other
than OCPs in order to lessen her risks for a subsequent stroke. Smoking and OCPs are known causes of hypercoagulability that can
lead to ischemic stroke. Accordingly, diet and exercise would also be important, as she would want to minimize her risks for future
diabetes and hypercholesterolemia. If this patient’s etiology is determined to be from hypercoagulability, she may benefit from
chronic anticoagulation/antiplatelet therapy from such agents as asprin, plavix, aggrenox, or coumadin.

4.a. This patient’s severe HA, syncope, and vomiting was most likely caused by a subarachnoid hemorrhage, which are most often the
result of a ruptured aneurysm in an intracranial blood vessel, but can also be the result of an AV malformation.

4.b. The differential diagnosis of a subarachnoid hemorrhage includes a ruptured berry aneurysm, AV malformation, coagulopathy
secondary to warfarin therapy, Vitamin K deficiency, thrombocytopenia, or a consumptive coagulopathy, infectious endocarditis, or
vasculitis. Other causes of this patient’s headache could include trauma, meningitis, hematoma, or just a severe headache.

4.c. Once the patient is stabilized, a CT scan should be performed immediately, as it is the optimal diagnostic study for detecting
hemorrhage and is easier to interpret than MRI. If the CT scan reveals no abnormality and a subarachnoid hemorrhage is still
suspected, a lumbar puncture should be performed immediately and the supernatant examined for RBCs and xanthochromia. Once
these are complete, if the diagnosis is still in question, other routine diagnostic tests can be performed such as dw-MRI, CBC, platelet
count, ESR, EKG, echocardiogram, etc.

4.d. Assuming the CT scan in this patient is diagnostic of a subarachnoid hemorrhage, this patient should be considered a medical
emergency, and if left untreated this patient has a 30-day fatality rate of 60%. Overall prognosis is relatively poor, with a 35-50%
mortality rate even with early, aggressive treatment. Aggressive treatment is warranted to stop the bleeding and prevent herniation,
and endovascular clipping or coiling if aneurysm is the etiology of the hemorrhage. Also, stabilization in the ICU should include
maintenance of blood pressure with fluids, pressors, and nicardipine, seizure prophylaxis, and continuous cardiac monitoring, with
angiography performed once the patient is stable.

				
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