CMS Neuro 4 Answers

7/25/2019 CMS Neuro 4 Answers

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NEURO FORM 4 by Sergio Angulo

1 E

2 E

3 A4 B

5 D

6 A

7 E

8 E

9 B

10 E

11 G

12 G

13 E

14 C15 C

16 E

17 B

18 B

19

20 B

21 E

22 A

23 C

24 C25 A

26 F

27 E

28 C

29 C

30 C

31 D

32 D

33 K

34 E

35 B36

37 A

38 D

39 E

40 A

41 C


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42 C

43 A

44 C

45 G

46 A

47 D48 A

49 C

50 A

1. E2. E

3. A4. B. looks like a hernia

5. D.normal opening pressure: 10-18 cm H2O in supine

glucose: 50-80 mg/dL

protein: 15-40 mg/dLRBC: negative

WBC: 0-3/mm3

The primary symptom of aneurysmal SAH is a sudden, severe headache(97 percent of cases) classically

described as the "worst headache of my life" [5]. The headache is lateralized in 30 percent of patients,

predominantly to the side of the aneurysm. Consistent with the rapid spread of blood, the symptoms of

SAH typically begin abruptly. Hypertension, cigarette smoking and family history are among the most

consistently observed risk factors
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Increased white blood cell (WBC) count, but usually less than 250/mm3.Thedifferential shows a predominance of lymphocytes, although early infection may reveal

a predominance of neutrophils. In the latter setting, a repeat CSF cell count eight hours

later will generally show a shift from neutrophils to lymphocytes [29].

Elevated protein concentration, but usually less than 150 mg/dL.

Usually normal glucose concentration (>50 percent of blood value), but moderately

reduced values are occasionally seen with HSV, mumps, or some enteroviruses. Red cells are usually absent (in a nontraumatic tap); their presence in the

appropriate clinical setting suggests HSV-1 infection or other necrotizingencephalitides.

6. A.

Neonates may have an abrupt onset of fever accompanied by nonspecific symptoms (eg, poor

feeding, vomiting, diarrhea, rash, respiratory symptoms). Neurologic manifestations may be

minimal, ranging from no symptoms, to irritability and lethargy, to frank nuchal rigidity or

bulging fontanelle [1,6,8]. Central nervous system (CNS) disease may progress to encephalitis

with seizures and/or focal neurologic findings [9]. Neonates are at increased risk for severe

systemic disease, particularly with herpes simplex virus (HSV).Systemic manifestations may

include pneumonia, hepatitis with necrosis, myocarditis, and necrotizing enterocolitis [9].Disseminated intravascular coagulation and other findings of sepsis can mimic overwhelming

bacterial infection.

Clinical manifestations of neonatal HSV CNS disease include seizures (focal or generalized),

lethargy, irritability, tremors, poor feeding, temperature instability, and full anterior

fontanel[28,30,31]. Early in the course of HSV CNS disease, none of these signs or symptoms

may be apparent.

In the absence of vesicles, the initial presentation of HSV CNS disease may be indistinguishable

from other causes of neonatal sepsis or meningitis [11,12]. Many experts recommend evaluation

for HSV CNS disease with HSV deoxyribonucleic acid (DNA) polymerase chain reaction (PCR)

and other CSF studies (ie, cell counts, protein, and glucose), and empiric treatment with

acyclovirin all neonates with aseptic meningitisor other signs and symptoms ofmeningoencephalitis without an obvious bacterial cause

Early intravenous administration of glucocorticoids (usuallydexamethasone)has been

evaluated as adjuvant therapy in an attempt to diminish the rate of hearing loss and other

neurologic complications as well as mortality in selected patients withbacterial meningitis.

The effects ofdexamethasoneon viral meningitis are not fully known; very few studies have

examined the long-term outcome of children with viral meningitis who may have received

dexamethasone at the time of presentation when bacterial meningitis was a consideration

Glucose (mg/dL) Protein (mg/dL)Total white blood cell count

(cells/microL)

1000 100 to 1000 5 to 100

More

common

Bacterial

meningitis

Bacterial

meningitis

Bacterial

meningitis

Viral meningitis

Nervous system

Lyme disease

(neuroborreliosis)

Bacterial

meningitis

Bacterial or

viral

meningitis

TB

meningitis

Early bacterial

meningitis

Viral

meningitis
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Neurosyphilis

TB meningitis

Neurosyphilis

TB meningitis

PathogenWBC

(cells/mm3)RBC

Glucose

(mg/dL)

Protein

(mg/dL)Viral diagnosis

Enterovirus 100-1000 None NL/SL


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8. E9. B10.E

11.G12.G

13.E14.C15.C

Carotid sinus hypersensitivity. Hypersensitivity of the afferent or efferent limbs of the carotid sinus reflex

arc results in vagal activation and/or sympathetic inhibition, which leads to bradycardia and/or

vasodilation; this is also called the carotid sinus syndrome or carotid sinus syncope.

Carotid sinus syncope is similar to vasovagal (neurocardiogenic) syncope since both are forms of reflex

syncope reflecting alterations in autonomic tone with similar clinical manifestations. However,

precipitating factors for these two types of syncope differ and carotid sinus hypersensitivity tends to

occur in older patients.

A history of syncope following accidental manipulation of the carotid sinuses should be sought although it

is rarely present. Absence of such a history does not exclude carotid sinus syndrome.

Vasovagal syncope:

Patients with vasovagal syncope are most commonly young and otherwise healthy. Typical triggers and

premonitory symptoms are strongly suggestive of vasovagal syncope, although these may be absent or

difficult to correlate to the syncopal episode. Women and patients younger than 40 are more likely to have

typical symptoms [25]. However, older patients are also frequently diagnosed with vasovagal syncope [26].

Older individuals have specific triggers that may be absent in younger individuals (ie, micturition, cough,

defecation, deglutition).

Vasovagal syncope (classical) refers to syncope triggered by emotional or orthostatic stress such as

venipuncture (experienced or witnessed), painful or noxious stimuli, fear of bodily injury, prolonged

standing, heat exposure, or exertion

Vasovagal syncope is often associated with a prodrome and persistence of nausea, pallor, and diaphoresis,

consistent with increased vagal tone. Syncope is typically of short duration and occurs in the sitting or

standing position. The supine position restores adequate blood flow to the brain. However, full recovery

may be delayed, as the patient may feel depressed or fatigued. This course may help distinguish vasovagal

syncope from syncope associated with arrhythmia, which is typically of abrupt onset and of short duration.

Loss of consciousness may be prolonged with some other causes of syncope, such as seizures and aortic

stenosis, but rarely with vasovagal syncope.

16. E

Vascular dementia

Patients with cognitive impairment and clinical or radiologic evidence of

cerebrovascular pathology should be screened and treated for vascular


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risk factors, especially hypertension, although this may be more helpful in

preventing rather than ameliorating dementia.

Antiplatelet agentsWhile of established efficacy in secondary stroke

prevention, no randomized trials have found a benefit foraspirinor other

antiplatelet therapy in the prevention or treatment of VaD [39]. The Aspirin forAsymptomatic Atherosclerosis (AAA) trial randomly assigned 3350 participants

(50 to 75 years) to aspirin or placebo, but after five years of follow-up, there

was no difference in cognitive test scores between the groups [40]. Other trials

comparing antiplatelet agents to each other have also found no benefit on

cognitive function or recurrent lacunar stroke

Evidence that specific treatments with acetylcholinesterase inhibitors and/or

memantine are helpful in VaD is not conclusive. However, it is reasonable to use

them in patients with suspected VaD because of the high prevalence of

comorbid Alzheimer disease (AD) and the difficulty of reliably distinguishing

between the primary etiologic entities. (See 'Disease modifying therapy' above.)

A typical regimen aimed to improve symptoms in VaD is donepezil 10 mg/day

plus memantine 20 mg/day; however, there are no data supporting the use of

one acetylcholinesterase inhibitor over another.

Cortical syndromeIn primarily cortical VaD, cognitive features are specific to

the areas affected [106]:

Medial frontal: executive dysfunction, abulia, or apathy. Bilateral medialfrontal lobe infarction may cause akinetic mutism.

Left parietal: aphasia, apraxia, or agnosia.

Right parietal: hemineglect (anosognosia, asomatognosia), confusion,agitation, visuospatial and constructional difficulty.

Medial temporal: anterograde amnesia.

Cortical branch occlusions are often caused by embolism from the heart or large

arteries and may present with clinical stroke. However, when the superior

division of the middle cerebral artery is not involved, hemiparesis may not be an

obvious signal that stroke has occurred. Onset may appear more insidious as a

result, and it is not uncommon for the patient to improve again before the next

event. The course is thus often perceived as fluctuating or stepwise. As few as

one-third of patients with multi-infarct dementia (MID) experience both an

abrupt onset and stepwise deterioration [107].
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Subcortical syndromeIn subcortical pathology, both lacunar infarctions and

chronic ischemia affect the deep cerebral nuclei and white matter pathways.

These often disrupt frontal lobe and other cortico-cortico circuits, producing

deficits attributable to remote brain areas [96,106,108,109]. Characteristic

features include:

Focal motor signs

Early presence of gait disturbance (marche a petit pas or magnetic,apraxic gait or Parkinsonian gait)

History of unsteadiness and frequent, unprovoked falls

Early urinary frequency, urgency, and other urinary symptoms notexplained by urologic disease

Pseudobulbar palsy

Personality and mood changes, abulia, apathy, depression, emotionalincontinence [110]

Cognitive disorder characterized by relatively mild memory deficit,

psychomotor retardation, and abnormal executive function [111]

The course of subcortical VaD may be gradual or stepwise and either slow or

fast in decline.

MRI will show the fundamental hallmarks of VaD including cortical and

subcortical infarctions as well as the presence of subcortical ischemic

changes or leukoaraiosis. However, radiographic criteria alone have been

shown to be inadequate at differentiating between poststroke patients

with and without dementia.

17.BMigraine prophylaxis.

In the absence of contraindications, we preferamitriptyline,one of the

beta blockers (metoprolol,propranolol,ortimolol), ortopiramatefor

initial treatment. For women of childbearing age, reasonable optionsincludeverapamilorflunarizine.In this group,valproateis problematic

because it is teratogenic and is associated with an increased risk of birth

defects. However, it can be considered for women utilizing effective

contraception if other options are not effective or tolerated.

18.B19. None
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20.B21.E

Arterial TOS Symptoms of arterial compression are the least common type of thoracic outlet syndrome,

accounting for only about 1 percent of cases. Symptoms develop spontaneously unrelated to work or

trauma [1]. Arterial TOS (aTOS) is almost always associated with a cervical rib or anomalous rib. It occurs

in young patients without typical atherosclerotic risk factors distinguishing it from peripheral arterydisease. (See"Overview of upper extremity peripheral artery disease".)

Hand ischemia with symptoms of pain, pallor, paresthesia, and coldness is the most common presentation.

Magnetic resonance Contrast-enhanced magnetic resonance (MR) angiography using provocative arm

positioning can allow excellent imaging to the vessels and can be a useful diagnostic tool.

22.A

Multiple sclerosis affects more women than men; the estimated female-to-male ratio of MS incidence is

approximately 2:1, with some data suggesting the ratio is even higher. The median and mean ages of MS

onset are 23.5 and 30 years of age, respectively. The peak age of onset is about five years earlier for womenthan for men. Onset of MS can rarely occur as late as the seventh decade. (See'Epidemiology and risk

factors'above.)

Genetic factors appear to contribute to the risk of MS, especially variation involving the HLA-DRB1 locus. (See'Genetic susceptibility'above.)

Although many viruses, and particularly the Epstein-Barr virus, have been associated with MS,there is no specific evidence linking viruses directly to the development of MS. (See'Viral

infections'above.)

The incidence and prevalence of MS vary geographically. The incidence and prevalence of MSvaries geographically [112,113]. High frequency areas of the world (prevalence of 60 per 100,000

or more) include all of Europe (including Russia), southern Canada, northern United States, New

Zealand, and southeast Australia.. This geographic variance was previously thought to be

explained in part by racial differences; white populations, especially those from NorthernEurope, appeared to be most susceptible, while people of Asian, African, or American Indian

origin appeared to have the lowest risk, with other groups intermediate. However,

subsequent studies in the United States demonstrated an increased incidence of MS in black

adults [114,115]and children [116], suggesting that this racial susceptibility may be

changing

There is an inverse relationship between sun exposure, ultraviolet radiation exposure, or serumvitamin D levels, and the risk or prevalence of MS. (See'Sunlight and vitamin D'above.)

There is no association between vaccines and the risk of MS.

23.CMyophosphorylase deficiency (McArdle disease, glycogen storage disease V [GSD V])

usually presents in adolescence or early adulthood with exercise intolerance,fatigue, myalgia, cramps, poor endurance, muscle swelling, and fixed weakness [1,4].

Typical laboratory findings include myoglobinuria and elevated creatinine kinase

(CK). The presentation is somewhat different in older adults and very young

children. Older patients may present with progressive weakness without history of

cramps or myoglobinuria.

24.C
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Diabetic retinopathy. Each year in the United States, diabeticretinopathy accounts for 12% of all new cases of blindness. It is alsothe leading cause of blindness for people aged 20 to 64 years.[5].Evenmacular edema,which can cause rapid vision loss, may nothave any warning signs for some time. In general, however, a personwith macular edema is likely to have blurred vision, making it hard todo things like read or drive. In some cases, the vision will get better orworse during the day.In the first stage which is called non-proliferative diabetic retinopathy(NPDR) there are no symptoms, the signs are not visible to the eyeand patients will have20/20 vision.The only way to detect NPDR isbyfundus photography,in whichmicroaneurysms(microscopicblood-filled bulges in the artery walls) can be seen. If there is reducedvision,fluoresceinangiographycan be done to see the back of the

eye. Narrowing or blocked retinal blood vessels can be seen clearlyand this is called retinalischemia(lack of blood flow).Macular edema in which blood vessels leak their contents into themacular region can occur at any stage of NPDR. The symptoms ofmacular edema are blurred vision and darkened or distorted imagesthat are not the same in both eyes. Ten percent (10%) of diabeticpatients will have vision loss related to macular edema.OpticalCoherence Tomographycan show the areas of retinal thickening(due to fluid accumulation) of macular edema.[6]In the second stage, abnormal new blood vessels(neovascularisation) form at the back of the eye as part ofpro l i ferat ive diabetic ret inopathy(PDR); these can burst andbleed (vitreous hemorrhage)and blur the vision, because thesenew blood vessels are fragile. The first time this bleedingoccurs, it may not be very severe. In most cases, it will leave justa few specks ofblood,or spots floating in a person's visualfield, though the spots often go away after a few hours.These spots are often followed within a few days or weeks by amuch greater leakage of blood, which blurs the vision. In

extreme cases, a person may only be able to tell light from darkin that eye. It may take the blood anywhere from a few days tomonths or even years to clear from the inside of the eye, and insome cases the blood will not clear. These types of largehemorrhages tend to happen more than once, often duringsleep.
https://en.wikipedia.org/wiki/Macular_edemahttps://en.wikipedia.org/wiki/Macular_edemahttps://en.wikipedia.org/wiki/Macular_edemahttps://en.wikipedia.org/wiki/20/20_visionhttps://en.wikipedia.org/wiki/20/20_visionhttps://en.wikipedia.org/wiki/20/20_visionhttps://en.wikipedia.org/wiki/Fundus_photographyhttps://en.wikipedia.org/wiki/Fundus_photographyhttps://en.wikipedia.org/wiki/Fundus_photographyhttps://en.wikipedia.org/wiki/Microaneurysmhttps://en.wikipedia.org/wiki/Microaneurysmhttps://en.wikipedia.org/wiki/Microaneurysmhttps://en.wikipedia.org/wiki/Fluoresceinhttps://en.wikipedia.org/wiki/Fluoresceinhttps://en.wikipedia.org/wiki/Angiographyhttps://en.wikipedia.org/wiki/Angiographyhttps://en.wikipedia.org/wiki/Angiographyhttps://en.wikipedia.org/wiki/Ischemiahttps://en.wikipedia.org/wiki/Ischemiahttps://en.wikipedia.org/wiki/Ischemiahttps://en.wikipedia.org/wiki/Optical_Coherence_Tomographyhttps://en.wikipedia.org/wiki/Optical_Coherence_Tomographyhttps://en.wikipedia.org/wiki/Optical_Coherence_Tomographyhttps://en.wikipedia.org/wiki/Optical_Coherence_Tomographyhttps://en.wikipedia.org/wiki/Vitreous_hemorrhagehttps://en.wikipedia.org/wiki/Vitreous_hemorrhagehttps://en.wikipedia.org/wiki/Vitreous_hemorrhagehttps://en.wikipedia.org/wiki/Bloodhttps://en.wikipedia.org/wiki/Bloodhttps://en.wikipedia.org/wiki/Bloodhttps://en.wikipedia.org/wiki/Sleephttps://en.wikipedia.org/wiki/Sleephttps://en.wikipedia.org/wiki/Sleephttps://en.wikipedia.org/wiki/Bloodhttps://en.wikipedia.org/wiki/Vitreous_hemorrhagehttps://en.wikipedia.org/wiki/Optical_Coherence_Tomographyhttps://en.wikipedia.org/wiki/Optical_Coherence_Tomographyhttps://en.wikipedia.org/wiki/Ischemiahttps://en.wikipedia.org/wiki/Angiographyhttps://en.wikipedia.org/wiki/Fluoresceinhttps://en.wikipedia.org/wiki/Microaneurysmhttps://en.wikipedia.org/wiki/Fundus_photographyhttps://en.wikipedia.org/wiki/20/20_visionhttps://en.wikipedia.org/wiki/Macular_edema


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Age-related macular degeneration (AMD) is a degenerative disease of the central portion of the retina (the

macula) that results primarily in loss of central vision. Central vision is required for activities such as

driving, reading, watching television, and performing activities of daily living.

AMD is classified as dry (atrophic) or wet (neovascular or exudative) for clinical purposes. Different

classifications and grading schemes have been used in epidemiologic and therapeutic studies of AMD.

Many epidemiologic studies make a distinction between age-related maculopathy (ARM) and age-related

macular degeneration (AMD). All wet lesions are AMD, but early dry lesions that do not reduce vision may

be classified as ARM rather than AMD. A further source of confusion is that AMD is often abbreviated asARMD.

The finding of either large soft drusen or RPE pigmentary clumping increases the risk of wet AMD. Wet

AMD is characterized by growth of abnormal vessels into the subretinal space, usually from the choroidal

circulation and less frequently from the retinal circulation [13]. These abnormal blood vessels leak, leading

to collections of subretinal fluid and/or blood beneath the retina (figure 1andpicture 4andpicture 5). Wet

type AMD is also referred to as choroidal neovascularization.

Wet AMD is more common than dry AMD among patients with advanced AMD [14]. Although wet

AMD is found in only 10 to 15 percent of patients with AMD, wet AMD accounts for more than 80

percent of cases with severe visual loss or legal blindness [10]. In contrast to dry AMD, in which

vision loss is slow and gradual, wet AMD is characterized by rapid distortion and loss of central

vision over a period of weeks to months.

In wet AMD, dilated examination may reveal subretinal fluid and/or hemorrhage

(picture 4). Neovascularization appears as a grayish-green discoloration in the

macular area (picture 5). The presence of subretinal hemorrhage or a gray

subretinal membrane is strongly suggestive of a subretinal choroidal membrane.

These patients require an office-basedfluoresceinangiogram delineate and
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characterize the neovascular membrane and optical coherence tomography to

identify the presence of subretinal fluid or retinal edema.

25.A26.F27.E

28.CAneurysmsof the posteriorcommunicatingartery are the thirdmost common circle of Willisaneurysm[1](the most common areanterior communicating arteryaneurysms) and can lead tooculomotor nervepalsy.Aneurysmsof the anterior communicating artery are the mostcommon circle of Willis aneurysm[1]and can causevisual field defectssuch asbitemporal heteronymous hemianopsia(due to compressionof theoptic chiasm),[2]psychopathologyandfrontal lobepathology.[3]

29.C30.C

REM sleep behavior disorder (RBD) is another nocturnal disorder commonly

seen in patients with PD [96]. This disorder is characterized by vigorous

movements that are related to increased muscle tone during REM sleep

[97]. Patients with RBD often act out their dreams and exhibit

vocalizations as well as flailing, kicking, and punching motions of the
https://en.wikipedia.org/wiki/Cerebral_aneurysmhttps://en.wikipedia.org/wiki/Cerebral_aneurysmhttps://en.wikipedia.org/wiki/Aneurysmhttps://en.wikipedia.org/wiki/Aneurysmhttps://en.wikipedia.org/wiki/Aneurysmhttps://en.wikipedia.org/wiki/Anterior_communicating_arteryhttps://en.wikipedia.org/wiki/Anterior_communicating_arteryhttps://en.wikipedia.org/wiki/Oculomotor_nervehttps://en.wikipedia.org/wiki/Paralysishttps://en.wikipedia.org/wiki/Paralysishttps://en.wikipedia.org/wiki/Paralysishttps://en.wikipedia.org/wiki/Aneurysmhttps://en.wikipedia.org/wiki/Aneurysmhttps://en.wikipedia.org/wiki/Visual_field_losshttps://en.wikipedia.org/wiki/Visual_field_losshttps://en.wikipedia.org/wiki/Visual_field_losshttps://en.wikipedia.org/wiki/Bitemporal_hemianopsiahttps://en.wikipedia.org/wiki/Bitemporal_hemianopsiahttps://en.wikipedia.org/wiki/Bitemporal_hemianopsiahttps://en.wikipedia.org/wiki/Optic_chiasmhttps://en.wikipedia.org/wiki/Optic_chiasmhttps://en.wikipedia.org/wiki/Psychopathologyhttps://en.wikipedia.org/wiki/Psychopathologyhttps://en.wikipedia.org/wiki/Psychopathologyhttps://en.wikipedia.org/wiki/Frontal_lobehttps://en.wikipedia.org/wiki/Frontal_lobehttps://en.wikipedia.org/wiki/Frontal_lobehttps://en.wikipedia.org/wiki/Frontal_lobehttps://en.wikipedia.org/wiki/Psychopathologyhttps://en.wikipedia.org/wiki/Optic_chiasmhttps://en.wikipedia.org/wiki/Bitemporal_hemianopsiahttps://en.wikipedia.org/wiki/Visual_field_losshttps://en.wikipedia.org/wiki/Aneurysmhttps://en.wikipedia.org/wiki/Paralysishttps://en.wikipedia.org/wiki/Oculomotor_nervehttps://en.wikipedia.org/wiki/Anterior_communicating_arteryhttps://en.wikipedia.org/wiki/Aneurysmhttps://en.wikipedia.org/wiki/Cerebral_aneurysm


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limbs. Some patients may injure themselves or their bed partners.

Behaviors related to RBD are reported to occur in 15 to 47 percent of

patients with PD [96,98,99], and over three-quarters of spontaneous RBD

cases eventually develop PD or other alpha-synucleinopathies, often years

after the onset of RBD.

Polysomnography is necessary for definitive diagnosis of RBD and to

exclude other sleep disorders that can mimic RBD.

31.DMyotonic dystrophy type 1 (DM1) and type 2 (DM2) are similar in that both are

multisystem disorders characterized by skeletal muscle weakness and myotonia,

cardiac conduction abnormalities, cataracts, testicular failure,

hypogammaglobulinemia, and insulin resistance.

However, DM2 is generally a less severe disease than DM1. In addition, there are

congenital, juvenile, and adult onset forms of DM1, whereas adult onset (typically in

the fourth decade) is the most common presentation for DM2 [10,26]. Nevertheless,there is a wide range of symptom onset in DM2 for myotonia (range 13 to 67 years,

median 30) and weakness (range 18 to 66 years, median 41)

Premature, male-pattern frontal balding is seen in both DM1 and DM2.

Type of DM Cataracts Cardiac abnormalities

Cognitive

impairment;

personality

disturbance

Endocrine

disturbance

Gastrointestinal

disorder

DM I

(Steinert's

disease)

Very

common;almost

universal

late in

course*

Conduction

disturbances well

recognized and

common late in

course*

Progressive

cardiomyopathy also

described

Mental retardation

(congenital form)

is common; mildto moderate

cognitive and

personality

defects in adult

form

Glucose

intolerance: well

recognized and

common late incourse*

Hypogonadism:

common and

almost universal

late in course*

Irritable bowelsymptoms;

dysphagia; gall

stones

DM II

(Proximal

myotonic

myopathy)

Common

(78% in

subjects

>50 years)

Conduction

disturbances less

problematic than DM

I (19 percent when

considered across age

spectrum [21 - >50])

Progressive

cardiomyopathy also

described

Mild cognitive

impairment may

be seen

Glucose

intolerance:

common, seen in

75 percent

Hypogonadism:

seen in 29 percent

Yes, but not as

pronounced as in

DM1; dysphagia

common butrelatively mild

Clinical Feature DM1* DM2, percent

Weakness
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Neck flexion +++ 75

Facial muscles ++ 12

Hip flexion + 64

Thumb/finger deep flexors +++ 55

Ankle dorsiflexion ++ 16

Shoulder abductors ++ 20Elbow extension ++ 31

Myotonia on examination +++ 75

Cataracts ++ 60

Spinal ms athrophydisorders are characterized by degeneration of the

anterior horn cells in the spinal cord and motor nuclei in the lower

brainstem. These diseases are classified as types 1 through 4 depending

upon the age of onset and clinical course. Patients with all forms of SMA

have diffuse symmetric proximal muscle weakness that is greater in

the lower than upper limbs and absent or markedly decreased deep

tendon reflexes

Facioscapulohumeral muscular dystrophy(FSHD) is the third most

common type of muscular dystrophy. It is a complex genetic disorder

characterized in most cases by slowly progressive muscle weakness

involving the facial, scapular, upper arm, lower leg, and hip girdle muscles,

usually with asymmetric involvement. The age of symptom onset varies from

infancy to middle age, but is usually in the second decade. By age 20 years,

findings are seen in approximately 90 percent of affected patients [4],

although some or all of the signs may be subclinical [26]. Progression is

usually slow with a normal or near-normal life span.

32.D

In vitro studies have also shown that terbinafine inhibits CYP2D6-mediated metabolism.This may be of clinical relevance for compounds predominantly metabolized by this

enzyme, such as tricyclic antidepressants, -blockers, selective serotonin reuptakeinhibitors (SSRIs), and monoamine oxidase inhibitors (MAO-Is) Type B, if they have a

narrow therapeutic window.Epileptic seizuresare the most importantadverse effect of bupropion.

Bupropion acts as annorepinephrine-dopamine reuptake inhibitor

(NDRI), and it serves as an atypical antidepressant different frommost commonly prescribed antidepressants such asselectiveserotonin reuptake inhibitors(SSRIs).

The only problem with this is that Bupropion is also an inhibitor ofCYP2D6. Bupropion is metabolized by CYP2B6.
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The core feature of catatonia is a motor disturbance in which patients are unable to move normally despite

full physical capacity in the limbs and trunk [1]. The disturbance can range from marked reduction in

movements to marked agitation. Starting, stopping, and planning movement can be impaired, and motor

behavior may be repetitive, purposeless, impervious to external stimuli, and contrary to intent [11].

Although catatonia can occur in the context of many mental disorders, it is most often found in [2,39-42]:

Bipolar I disorder

Bipolar II disorder

Unipolar major depression (major depressive disorder)

Psychotic disorderso Schizophreniao Schizoaffective disordero Brief psychotic disordero Schizophreniform disorder

Autism spectrum disorder

Delirium

33.K

The superficial branch of theradial nervepasses along the front of the radial side of theforearmto the

commencement of its lower third. It is a sensory nerve.

It lies at first slightly lateral to the radial artery, concealed beneath the Brachioradialis.In the middle third

of the forearm, it lies behind the same muscle, close to the lateral side of the artery.

It quits the artery about 7 cm. above the wrist, passes beneath the tendon of the Brachioradialis, and,

piercing the deep fascia, divides into two branches: lateral and medial.
http://www.uptodate.com/contents/catatonia-in-adults-epidemiology-clinical-features-assessment-and-diagnosis/abstract/1http://www.uptodate.com/contents/catatonia-in-adults-epidemiology-clinical-features-assessment-and-diagnosis/abstract/1http://www.uptodate.com/contents/catatonia-in-adults-epidemiology-clinical-features-assessment-and-diagnosis/abstract/1http://www.uptodate.com/contents/catatonia-in-adults-epidemiology-clinical-features-assessment-and-diagnosis/abstract/11http://www.uptodate.com/contents/catatonia-in-adults-epidemiology-clinical-features-assessment-and-diagnosis/abstract/11http://www.uptodate.com/contents/catatonia-in-adults-epidemiology-clinical-features-assessment-and-diagnosis/abstract/11https://en.wikipedia.org/wiki/Radial_nervehttps://en.wikipedia.org/wiki/Radial_nervehttps://en.wikipedia.org/wiki/Radial_nervehttps://en.wikipedia.org/wiki/Forearmhttps://en.wikipedia.org/wiki/Forearmhttps://en.wikipedia.org/wiki/Forearmhttps://en.wikipedia.org/wiki/Brachioradialishttps://en.wikipedia.org/wiki/Brachioradialishttps://en.wikipedia.org/wiki/Brachioradialishttps://en.wikipedia.org/wiki/Brachioradialishttps://en.wikipedia.org/wiki/Forearmhttps://en.wikipedia.org/wiki/Radial_nervehttp://www.uptodate.com/contents/catatonia-in-adults-epidemiology-clinical-features-assessment-and-diagnosis/abstract/11http://www.uptodate.com/contents/catatonia-in-adults-epidemiology-clinical-features-assessment-and-diagnosis/abstract/1


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34.E?

This one is very confusing

Side effects, especially with higher doses, include dizziness,drowsiness, fatigue, diarrhea, unusual dreams,ataxia,troublesleeping, depression, and vision problems. It may also reduce blood

flow to the hands and feet, causing them to feel numb and cold;smoking may worsen this effect.[16]Due to the high penetration acrosstheblood-brain barrier,lipophilicbeta blockers such aspropranololand metoprolol are more likely than other less lipophilic beta blockersto cause sleep disturbances such as insomnia and vivid dreams andnightmares.[17]Serious side effects that are advised to be reported immediately
https://en.wikipedia.org/wiki/Ataxiahttps://en.wikipedia.org/wiki/Ataxiahttps://en.wikipedia.org/wiki/Ataxiahttps://en.wikipedia.org/wiki/Blood-brain_barrierhttps://en.wikipedia.org/wiki/Blood-brain_barrierhttps://en.wikipedia.org/wiki/Blood-brain_barrierhttps://en.wikipedia.org/wiki/Lipophilichttps://en.wikipedia.org/wiki/Lipophilichttps://en.wikipedia.org/wiki/Lipophilichttps://en.wikipedia.org/wiki/Propranololhttps://en.wikipedia.org/wiki/Propranololhttps://en.wikipedia.org/wiki/Propranololhttps://en.wikipedia.org/wiki/Propranololhttps://en.wikipedia.org/wiki/Lipophilichttps://en.wikipedia.org/wiki/Blood-brain_barrierhttps://en.wikipedia.org/wiki/Ataxia


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include symptoms ofbradycardia(resting heart rate slower than 60beats per minute), persistent symptoms of dizziness, fainting andunusual fatigue, bluish discoloration of the fingers and toes,numbness/tingling/swelling of the hands or feet,sexual dysfunction,erectile dysfunction(impotence), hair loss, mental/mood changes,depression, trouble breathing, cough,dyslipidemia,and increasedthirst. Taking it with alcohol might cause mild body rashes, so is notrecommended.

35.B36.None37.A38.D39.E40.A

41.C

Toxoplasma encephalitis Toxoplasma encephalitis (TE) represents reactivation disease from prior

infection. Affected patients present with fever, headache, altered mental status, and focal neurologic

complaints or seizures. Supporting laboratory findings include the presence of Toxoplasma antibodies,

which is consistent with past exposure, and advanced immunosuppression with CD4 counts 4 cm) lesions are

more suspicious for primary CNS lymphoma.

The initial therapy of choice for TE consists of the combination of

pyrimethamine plus sulfadiazine plus leucovorin(AI) (203--206).

Pyrimethamine penetrates the brain parenchyma efficiently even in

the absence of inflammation (207). Use of leucovorin reduces the

likelihood of the hematologic toxicities associated withpyrimethamine therapy (208,209). The preferred alternative

regimen for patients with TE who are unable to tolerate or who fail

to respond to first-line therapy is pyrimethamine plus clindamycin

plus leucovorin(AI)(203,204).
https://en.wikipedia.org/wiki/Bradycardiahttps://en.wikipedia.org/wiki/Bradycardiahttps://en.wikipedia.org/wiki/Bradycardiahttps://en.wikipedia.org/wiki/Sexual_dysfunctionhttps://en.wikipedia.org/wiki/Sexual_dysfunctionhttps://en.wikipedia.org/wiki/Sexual_dysfunctionhttps://en.wikipedia.org/wiki/Erectile_dysfunctionhttps://en.wikipedia.org/wiki/Erectile_dysfunctionhttps://en.wikipedia.org/wiki/Dyslipidemiahttps://en.wikipedia.org/wiki/Dyslipidemiahttps://en.wikipedia.org/wiki/Dyslipidemiahttp://www.uptodate.com/contents/toxoplasmosis-in-hiv-infected-patients?source=see_linkhttp://www.uptodate.com/contents/toxoplasmosis-in-hiv-infected-patients?source=see_linkhttp://www.uptodate.com/contents/toxoplasmosis-in-hiv-infected-patients?source=see_linkhttp://www.uptodate.com/contents/approach-to-hiv-infected-patients-with-central-nervous-system-lesions/abstract/10http://www.uptodate.com/contents/approach-to-hiv-infected-patients-with-central-nervous-system-lesions/abstract/10http://www.uptodate.com/contents/approach-to-hiv-infected-patients-with-central-nervous-system-lesions/abstract/10http://www.uptodate.com/contents/approach-to-hiv-infected-patients-with-central-nervous-system-lesions/abstract/10http://www.uptodate.com/contents/toxoplasmosis-in-hiv-infected-patients?source=see_linkhttps://en.wikipedia.org/wiki/Dyslipidemiahttps://en.wikipedia.org/wiki/Erectile_dysfunctionhttps://en.wikipedia.org/wiki/Sexual_dysfunctionhttps://en.wikipedia.org/wiki/Bradycardia


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Corticosteroid therapy should be considered in two settings:

When substantial mass effect can be demonstrated on imaging and the mental status is

significantly depressed. Such patients are at risk for cerebral herniation.

When the diagnosis of PCNSL has already been established, since steroids can cause false

negative results on a subsequent brain biopsy in patients with lymphoma.

42. C43. A

Adverse effects associated with anticholinergic use in older adults include memory impairment,

confusion, hallucinations, dry mouth, blurred vision, constipation, nausea, urinary retention, impaired

sweating, and tachycardia

44. C

Lumbosacral radiculopathy is often extremely painful. Analgesic medications such as nonsteroidal

anti-inflammatory drugs (NSAIDs) oracetaminophenand activity modification are the mainstay of

treatment. Physical therapy is often tried for patients with mild to moderate persistent symptoms, but

evidence of effectiveness is lacking.

The utility of systemic glucocorticoids and epidural glucocorticoids is limited.

For imaging of the lumbar spine, MRI, CT, and CT myelography (CT scan after intrathecal

administration of contrast media) are equally sensitive for the diagnosis of disc herniation [34]. For

routine initial assessment, an MRI (image 1andimage 2andimage 3)is more informative than CT

because it can also identify other intraspinal pathologies, including inflammatory, malignant, and

vascular disorders. In addition, MRI is not associated with ionizing radiation and is less invasive

than CT myelography.

For patients with persistent or severe findings in whom the etiology is not confirmed onneuroimaging, we suggest electromyography and nerve conduction studies

45.G46.A47.D48.A49.C

In patients who do not respond to nonpharmacologic therapy and

correction of iron deficiency, we recommend pharmacologic treatment with

a dopamine agonist (Ropirinole,, pramipexole) or an alpha-2-delta

calcium channel ligand Pregabalin, gabapentin) as first-line therapy(table 2). These classes of drugs have been shown to be effective compared

with placebo in multiple randomized controlled trials

50.A
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EXTRA Qs

A 72-year-old man is brought to the emergencydepartment because of a decreased level of

consciousness for the past 6 hours. Three days ago, hehad fever, shortness of breath, and productive coughtreated with an antibiotic, but his symptoms did not

improve. On arrival, his temperature is 39C (102.2F),

pulse is 110/min, respirations are 28/min, and bloodpressure is 110/75 mm Hg. Breath sounds are decreasedover the right midlung field. On neurologic examination,

he is unarousable but responds to tactile stimuli bymoaning. Cranial nerves are intact. There is resistance topassive flexion of the neck. Which of the following is the

most likely pathogen?

A) Herpes simplex virus 1

B) Listeria monocytogenesC)

Pseudomonas aeruginosa D) Streptococcus pneumoniae

E) Toxoplasma gondii

A 72-year-old man with a 3-year history of Parkinsondisease is brought to the physician by his wife for a

follow-up examination. Three weeks ago, his dosage ofcarbidopa-levodopa was increased. Since then, he hasreported seeing people spying on him from across the

street. He has no other history of serious medical orpsychiatric illness and takes no other medications.Physical examination shows a resting tremor. There is

cogwheel rigidity and increased muscle tone. On mental


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status examination, he reports seeing people spying on

him and says his wife is "one of them." Addition of whichof the following medications is the most appropriate nextstep in pharmacotherapy?

A) Haloperidol B) Lorazepam C) Paroxetine D)Quetiapine E) Valproic acid

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