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Neurology > Programs > > Clinical Case Studies


Clinical Case Studies

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These are clinical cases for you to work on.  The Library has the answers on reserve in the Clinical Case Study binders.

In order of presentation: 1 2 18 24 25 32 3 6 7 30 31 36 22 11 17 4 15 16 20 19 21 12 23 28 29 10 5 13 14 8 9 26 32 33 34 35 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 1a 2a 3a 4a 5a 6a 7a 8a 9a


A 52 yo AA hypertensive, diabetic, hypercholesterolemic man awakens and can not express himself. His entire right side is numb and weak. Neurologic exam shows a right hemiparesis (face, arm and leg are equal). Hemianesthesia is present and there is a Broca aphasia. The patient reports mild left temporal headache.

* A. What is the most likely mechanism?

* B. Which vessel territory is affected?

* C. Which imaging studies should be initially performed

* D. If motor and sensory impairment involved the arm and face but spared the leg would this     change your opinion?

* E. If the patient had no language impairment or sensory deficit, what would be the most probable lesion localization?

* F. If the initial patient described became lethargic and then comatose with fixed dilated left pupil and right hemiplegia, what would be your explanation?


A 46 yo caucasian woman develops right sided visual blurring, "disorientation," and left sided throbbing temporal headache without vomiting. She then develops right hand and facial numbness. Her past history is significant for hypercholesterolemia, angina treated with percutaneous coronary angioplasty 10 years ago, and she was recently started on Premarin (conjugated estrogens) for hot flashes. The family history is negative for stroke or migraine.

Neurologic exam reveals a right homonymous hemianopsia, right hemianesthesia (face and arm are equal, the leg is not as affected). The blood pressure is 140/90, HR=80. The cardiac, skin, lung exams are normal. Homan's sign is absent, there are no bruits.

    * Imaging studies CT reveals a temporal subarachnoid cyst.

    * MRI reveals multiple high signal cortical and subcortical lesions on the left side on T2 weighted images.

    * Carotid ultrasound reveals mild carotid stenosis bilaterally (<50%) without ulceration.

    * EEG is normal.

    * MRAngiography is normal

The total cholesterol is 231 with elevated LDL and decreased HDL.

During her course the headache resolves with Tylenol and 4 days later the neurologic exam is normal.

    * 1. Should angiography be performed? Why?

    * 2. Should a diagnosis of "complicated migraine" be made?

    * 3. Could the left temporal subarachnoid cyst be the causative lesion?

    * 4. Which meds should be considered?

          o Depakote (valproic acid)

          o verapamil

          o Plavix (clopidogrel)

          o Pravachol (pravastatin)

          o Aspirin

          o Persantine

          o Ticlid (ticlopidine)

          o Inderal (propranolol)

          o Coumadin (warfarin)

    * 5. Is a change in Premarin warranted?



A 67 year old hypertensive, diabetic, hypercholesterolemic, obese, sedentary man with prior history of coronary artery disease, peripheral vascular disease, and transient ischemic attack develops left facial numbness, vertigo and gait disequilibrium. This develops four days after an episode of emotional stress during which he is accused of causing a labor dispute involving his labor union.

Medications include Metformin (glucophage), Pravachol (pravastatin), metoprolol, verapamil, a thiazide diuretic, Imdur (isosorbide mononitrate), and Catapres (clonidine).

The past history is significant for transient ischemic attack, intermittent claudication and unstable angina.

The physical exam reveals BP 200/110, pulse 80. The neurologic exam reveals a broad based gait and a left Horner's syndrome. There is left facial and right body anesthesia, left dysmetria, decreased gag and palatal reflex, and dysarthria.

    * A. What is the neurologic disorder?

    * B. What is the lesion location?

    * C. What tests are warranted?

    * D. If seen within 3 hours of symptoms onset, what treatment could be given?

    * E. If seen within 6 hours, what treatment could be given?

    * F. What is the role of emotional stress in this disorder?



A 48 year old diabetic hypercholesterolemic woman has multiple transient right eye visual loss episodes (duration 15 minutes). She described these "as if a curtain is being pulled down." There are no other accompanying symptoms. The past history is significant for coronary artery disease with prior myocardial infarction, peripheral vascular disease with intermittent claudication, migraine with aura as an adolescent. The ovaries were removed surgically and she takes estrogen replacement hormones.

Neuro exam shows yellow refractile bodies within the retinal artery. An outside physician does not alter her treatment or perform ancillary studies. These episodes persist and one month later she awakens with a left sided hemiparesis and hemianesthesia.

    * A. What is the mechanism of visual symptoms?

    * B. How can you confirm this?

    * C. What would you expect pupils, visual field and extraocular muscle exam to show?

    * D. Outline the appropriate management on presentation.

    * E. What is anosagnosia of Babinski?



A 68 year old man with nonvalvular atrial fibrillation awakens one day and notices difficulty seeing on his right side; he has no difficulty with speech, walking, strength, sensation or coordination or headache.

The blood pressure is 110/80, pulse 80. The neurologic exam reveals a right homonymous hemianopsia. The heart is irregularly irregular and without murmurs. CT of the head is unremarkable.

The patient remains stable but a repeat CT three days later shows a hypodense left occipital lesion without mass effect and dense gyriform enhancement.

    * A. What is the mechanism of the visual impairment?

    * B. Where's the lesion?

    * C. What is the significance of the initial and subsequent CT findings?

    * D. What is the appropriate management strategy?



A 55 year old man undergoes 5 vessel coronary artery bypass grafting [CABG] for unstable angina. Prior to surgery he is found to have bilateral carotid bruits and duplex Doppler ultrasound shows 60% carotid stenosis belaterally. Brain CT and MRI show "bilateral periventricular abnormalities consistent with ischemic damage or demyelination." Following successful CABG, from which he makes a full and complete recovery, he undergoes bilateral carotid endarterectomy. Following this surgery, neurologic exam is nomral. He undergoes cardiac rehab and is pronounced fit to return to work in 6 weeks. At home, his wife initially supervises his bill paying, cooking and driving; she feels he is "okay." Three weeks after his return to work as a parmacist, he is terminated because he has made multiple "errors" and the patient has noted problems performing sequential tasks. His cardiologist evaluates him and on his mental state he has no abnormality, including 3 objects at 5 minutes, intact serial 7s and serial 3s. A psychiatric referral is suggested.

   1. What's the differential diagnosis?

   2. What other tests should be done?

   3. Could he have multi-infarct dementia?

   4. What is "pseudodementia?"



A 52 year old hypertensive, insulin-dependent diabetic man suddenly becomes mute and unable to express himself. His wife calls 911 and EMS arrives 10 minutes later. The patient can not express himself and has right hemiaresis (more in the arm than the leg). Despite the fact that glucose shows that he is not hypoglycemic, he is given 50 grams of glucose (an ampule of D50). He arrives at the hospital 20 minutes later. CT shows no abnormality. Recombinant tissue plasminogen activator (tPA) and he begins to speak and can move his right arm. Three days later, exam shows normal repetition and comprehension. Speech is nonfluent with low word output and agrammatical speech which is poorly articulated and without appropriate melody.

   1. What is wrong with this patient's speech?

   2. What has happened to this patient?

   3. Was there any potential danger in administering glucose to this patient?

   4. What might MRI show?



A 34 year old attorney wins a two million dollar judgment against a large HMO on Friday afternoon. After celebrating with champagne at Joe's that evening he experiences an episode of flashing lights beginning in his right visual field and moving slowly such that a "scotoma" follows this. Twenty minutes later the visual distrubance resolves and he develops left sided throbbing headache which builds up to maximal intensity over 3 hours. Activity makes the headache worse. He feels better lying down in a dark room. The past history is significant only for motion sickness as a child. His mother has hypertension and migraine headache. The neurologic exam is normal in the emergency room.

    * A. What diagnostic tests should be done?

    * B. What is the probable diagnosis?

    * C. What is the appropriate treatment?



A 25 year old electrician falls off a ladder and strikes his head. He is unconscious for 20 minutes; when he regains consciousness he has amnesia for the event, but is otherwise normal. He develops a dischage from his nose and hematoma encircling his eyes. The next day he has a temporal headache and vertigo when he sits up. He goes to an emergency room, where a skull roentgenogram is normal.

      He is afebrile. The neurologic exam reveals mild recent memory loss, anosmia, an ataxic gait. The neck is supple.

      He is discharged from the ED with Antivert (meclizine) and Fiorinal (aspirin, caffeine and butalbital); two days later his headache persists and he is febrile. The neurologic exam is normal except for anosmia.

          o A. What is wrong with this patient?

          o B. What is the next diagnostic test?

          o C. What is the risk of seizures occurring?



A 35 year old truck driver is involved in an MVA in which he strikes his head on the steering wheel. He is dazed and has a frontal bruise. He complains of headache and neck pain. Two days later, he reports an episode of feeling faint, light-headed and weak in his legs. He goes to the local Jiffy-Health Center (owned by a well-known HMO) and while being assessed by a nurse-receptionist he feels dizzy and passes out. The nurse observes right arm and left leg myoclonic jerks and he urinates on himself. Immediately after the episode, he is alert.

      The neurologic exam is entirely normal except for accomodative paresis. The remainder of the physical reveals spasm of the trapezius muscle and limitation of neck movement laterally; flexion is supple.

A. What is the most likely explanation for the "spells" and exam findings?

B. What should be the initial diagnostic studies?

C. If an EEG is abnormal due to "bitemporal theta activity" would this change your diagnosis?

D. Cervical spine MRI ordered by the trucking company shows "C5-6 disc protrusion." What would   you predict electromyography/nerve conduction studies of the upper extremities to show?

E. Define these terms:





                 psychogenic seizure




F. Can this patient return to truck driving?



A 25 year old man falls on a wet surface at Walgreens and lands on his buttock. He reports pain in the lower back and inability to walk straight, and demands to be taken to the Tulane ER. After a complete evaluation, he is found to be "normal" and referred to the neurology clinic. The following day he reports pain in his low back and entire left sided numbness and weakness. On neurologic exam

         1. Mental status is normal

         2. Gait -- dragging of the left foot, which is held stiffly

         3. Motor -- inability to squeeze examiner's finger or extend the left wrist; inability to dorsiflex or plantar flex the left foot.

         4. Reflexes are 2+ and symmetrical; plantar flexion to sole stimulation bilaterally

         5. Sensory -- absent pinprick and light touch on left; absent proprioception and vibration at all joints on the left side

         6. CN -- reduced heading in the left ear and colors appear less bright in the left eye

         1. Questions Where's the lesion?

         2. What is the mechanism?

         3. What tests should be done?

         4. Define

               1. conversion disorder

               2. Briquet syndrome

               3. somatoform disorder

               4. hysteria

         5. Could this patient have multiple sclerosis?



A 7 year old boy falls off a swing and hit his head on a rock and is knocked unconscious for ten minutes. Upon awakening he is neurologically intact but does not remember the accident. Several hours later, he develops a headache, vomits and develops right sided weakness.

         1. On exam BP 180/110 HR 50, RR 28 Mental status -- Lethargic but responsive

         2. Motor -- Right hemiparesis

         3. Reflexes bilateral plantar extensor response

         4. Cranial nerves -- left pupil is 8mm and poor reactive to light

         5. Fundi do NOT show spontaneous venous pulsations.

    * What happened to this boy?

    * What test should be done initially?

    * What treatment should be initiated?

    * Define the following:

         1. concussion

         2. diffuse axonal injury

         3. lucid interval

         4. transtentorial herniation

         5. tonsillar herniation

         6. whiplash injury

         7. lumbago

         8. sciatica



A 42 year old man is evaluated for back pain. This is an aching pain which radiates to his foot. he is uncomfortable walking and can not find a comfortable position in bed. He consults his primary care provider and is treated with pain medication, muscle relaxants and an NSAID. He is no better; percocet proves ineffective. He reports a tingling sensation over the top of his right foot and he has tripped on two occasions.

         1. Neuro exam shows absent right ankle jerk

         2. weaknes of dorsiflexion and plantar flexion

         3. decreased pinprick over the toop of the foot

         4. Loss of lumbar lordosis

         5. paraspinal muscle spasm in the lumbar region

         6. (+) Straight leg raise at 30 degrees on the right

         7. point tenderness over five lumbar vertebrae

         1. What structures are involved?

         2. What are potention mechanisms?

         3. What diagnostic studies are indicated?

         4. What are the clinical features of

               1. Brown-Sequard syndrome

               2. transverse [thoracic] myelitis

               3. anterior spinal artery ischemia

               4. conus medularis symdrome

               5. cauda equina syndrome?

               6. cervica syringomyelia



"Hurricane" Bill is mugged outside a bar in the French Quarter. He is unconscious for 15 minutes and has both anterograde and retrograde amnesia. The neurologic exam is normal except for abnormal olfaction. Ancillary studies include a skill roentgenogram which shows a linear parietal skull fraction. CT and MRI are normal.

      Six months later he experiences an episode of lost awareness. This begins with funny sensation in his stomach which then rises to his chest. He then smells "burning rubber," and his wife states he has rhythmical blinking. After three minutes he is confused and complains of a left temporal headache.

          o A. Has the patient suffered a concussion or a contusion?

          o B. Interictal EEG is normal. Does this patient has psudo-seizures?

          o C. A repeat interictal EEG shows left anterior temporal spikes. Does this patient have partial complex seizures?

          o D. Repeat MRI shows left hippocampal atrophy. What is the mechanism?



A 23 year old injection drug user develops myalgia, fever and bifrontal headache. One week ago he had a 3 day episode of diarrhea, which responded to symptomatic therapy and resolved spontaneously.

      On exam BP 140/80 HR 110 temperature 38.4C, respirations 12. The neck is supple and the skin is without rashes. The muscles are diffusely tender. The neurologic exam is normal.

      WBC=10,000, 60% lymph, 40% PMN. ESR=40, U/A and chest film are normal.

      A resident of a different speciality (and who tends to start patient descriptions with the phrase "this is the guy") believes "bacterial meningitis" or subarachnoid hemorrhage are likely possibilities (he does not consult neurology, a service he regularly belittles) and wants to ensure a nontraumatic tap. Since he read that the spinal interspaces are bigger higher up in the cord, he performs the tap at T9-10 instead of L3-4. Following this LP based on RANDO criteria (Resident Ain't Never Done One) the patient develops these imprairments:

         1. paraplegia with hypotonia

         2. absent patellar and ankle reflexes

         3. bilateral plantar responses

         4. a sensory loss to all modalities at T9

         5. incontinence.

          The ER staff asks you to answer the following questions so he can brief risk management

o  A. Explain the post LP neurologic findings
o B. What diagnostic studies are warranted?
o C. Are post-LP findings consistent with anterior spinal artery ischemia?
o D. Critique the initial handling of the case
o E. Should a CT have been performed prior to performing the LP? 


A 35 year old electrician is involved in an MVA where he is struck from behind. Mild low back pain resolves completely after two days. Four weeks later he begins to trip frequently, and three days after that he has difficulty climbing stairs and opening jars.
          o The neurologic exam reveals weakness of the feet, hips, legs, knees and hands.
          o He cannot walk on his toes or heels.
          o Reflexes are absent; there are plantar responses.
          o Sensation is normal
      The physical exam is otherwise normal.
         1. Impairment of which structures explains these findings? What diagnostic tests should be done?
         2. Three days later he develops diplopia and dyspnea. What might explain this?
         3. What are the treatment options?
         4. He shows clinical improvement. Lumbar MRI shows diffuse spinal and nerve root enhancement. What is the mechanism?
         5. What is the relationship of trauma to this condition?


A 30 year old hockey player is checked into the boards hard by the Flyers' Eric Lindros, striking his head and back, and briefly losing consciousness. (The rabid Philadelphia crowd goes wild.) He complains of occipital pain which is mild but also severe mid-thoracic back pain. Team physicians send him to the ER for observation. The following day the occipital pain is gone but the back pain persists and he reports a band of numbness on the left chest region extending to his back. He experiences difficulty urinating.

Neurologic exam reveals mild weakness in both legs; the arms are normal. Reflexes at the ankle,knee and abdominals are present but depressed, and there are plantar responses bilaterally. There is decreased perception of pinprick from the umbilicus downward, and there is a band of decreased seneation on the left mid thoracic and back region. There is a reduced anal wink.
         1. What was the mechanism of the initial injury?
         2. What condition could cause the symptoms and signs which developed the following day?
         3. What neuroimaging studies are warranted?
         4. Could the neurologic impairment be explained by subdural hematoma?


A 70 year old judge notes deterioration in his handwriting such that clerks can not read it. (See sample.) He also has difficulty cutting his food and bringing a cup to his mouth. He jokes that has always been shaky and that this runs in his family.

Neurologic exam reveals normal gait and station. There is a motor sustention and intention arm tremor; mild tremor of his voice but no rigidity or bradykinesia; Myerson's sign (-). A drawing of Archimedes spiral is presented.

         1. What is the differential diagnosis?
         2. What medication might cause this?
         3. What is the effect of Sinement (carbidopa/levodopa)?
         4. Define a treatment strategy for a Parkinson's patient with tremor.
         5. Outline a treatment strategy for a Parkinson's patient with tremor who is functionally impaired.
         6. List the major side effects for the following medications
                o Cogentin (benztropine)
                o Sinemet (carbidopa/levodopa)
                o Deprenyl (selegiline)
                o Parlodel (pergolide)



A 15 year old adolescent is described as being "nervous and fidgety" (more than appropriate for age, all things considered). His performance in school and his behavior become bizarre. Past history is significant for viral hepatitis 2 years ago and unexplained hemolytic anemia 4 years ago. Both his parents are diagnosed with schizophrenia.

      On exam he is inattentive with motor restlestness. The gait is broad based with impaired postural reflexes. Motor exam reveals cogwheel rigidity and intentional tremor. Finger-to-nose and heel-to-shin testing are impaired. The cranial nerves and fundi are normal. The physical exam reveals hepatosplenomegaly; the skin is normal.
         1. What are the diagnositic possibilities?
         2. What tests are warranted?
         3. What are the treatment options?
         4. What is the natural history of this condition if not treated?


A 70 year old physician is brought to a neurologist by his family because of "failing memory." He forgets to pay his bills, has lost his house keys and gotten lost while driving. Recently, three patients have initiated malpractice claims due to his failure to diagnose their condition correctly. He has become depressed and recently locked himself in the bathrom. He appears to move slowly and has suffered multiple recent falls.

Neurologic exam reveals a Mini-Mental Status Exam of 19/30. The gait is slow and he has difficulty initiating movement. Postural stability is impaired. Strength is normal and coordinated movements are slow. There is bilateral cogwheel rigidity but no tremor.

Gaze both up and down is impaired. Myerson's sign is present (+) and there is neck rigidity.

         1. What neurological impairments does this patient suffer from?
         2. What is the differential diagnosis?
         3. What studies are warranted?
         4. following initiation of Sinemet (carbidopa/levodopa) he become agitated, psychotic and has
             visual  hallucinations. What should be done?
         5. Discuss other treatment options.


A 40 year old injection drug user, while walking down the street minding his own business, is shot in the left orbit and the bullet damages the left frontal brain region. He undergoes bifrontal craniotomy for bullet removal and brain debridement. Following surgery, he is alert and attentive with no aphasia or memory impairment. He has no motor coordination, gait, hearing or visual disturbance (other than left eye blindness). He makes an uneventful recovery but his wife calls the neurosurgeon very upset. He refuses to return to work or pay any bills, goes to bars and Harrah's Casino and loses large sums of money, refuses to go to church and sexually abuses a 6 year old girl and is arrested for indecent exposure.
         1. Assuming this behavior is a dramatic step down from his life injecting drugs Explain the possible mechanism of this behavior which his wife says is a dramatic change
         2. What would neuro-psychiatric testing likely show?
         3. Who was Phineas Gage?


A 25 year old pregnant woman goes into active labor. She has a generalized seizure due to eclampsia. She is treated with fosphenytoin and magnesium sulfate and has no further seizures. During labor she receives generous amounts of fluid due to possible dehydration. Four hours later she is delivers a healthy baby girl by spontaneous vaginal delivery. In the recovery room she complains of generalized weakness which progressively worsens. Examination shows both proximal and distal weakness in her arms and legs, normal sensation and absent reflexes, normal cranial nerves. Over the next 24 hours this weakness progresses to quadriplegia with respiratory disturbances.

         1. What are potential mechanisms of the quadriplegia?
         2. What laboratory tests should be done?
         3. What neurodiagnostic tests should be done?
         4. Explain the significance of the finding of high signal intensity on MRI in (a)parietal-occipital subcortical region or (b)mid-pons.


An 18 year old man (HM) had a fall from his bicycle at age 6 and struck his head. He was unconscious for several hours. Skull roentgenogram showed a left parietal linear skull fracture. Six months later he had "staring spells" preceded by olfactory aura. Three months later he had generalized seizure. Despite treatment with multiple medications seizures occur on a daily basis. EEG shows bitemporal slow wave activity and right temporal spikes. MRI shows right temporal lobe atrophy. He undergoes right temporal lobectomy for seizure control. Following surgery he has no further seizures, but reports a problem with his memory. When the patient has breakfast he can not remember eating 15 minutes later. He talks to the examiner, but cannot remember the conversation 20 minutes later. His memory is generally impaired for recent but not remote events.
         1. What has happened?
         2. What neural structures account for memory loss in this patient?
         3. What is the memory circuit?


A 25 year old woman slips and falls in a shopping mall on a soap sample outside the Body Shop. She complains of low back pain which does not radiate down her legs. (Also, the soap smells terrible.) She calls her physician who calls in a prescription for an NSAID and a muscle relaxant. Five days later she continues to have severe pain and demands to see a neurologist.

      Neurologic exam reveals a broad based gait with difficulty standing on her heels. Romberg's sign is present. There is weakness of dorsiflexion and evertion of the feet. There is decreased vibration and position sense in the legs. Reflexes are absent in the ankles. The cranial nerves are normal. The general exam reveals high arched feet (of which the patient has always been proud), and hammer toes and pes cavus deformity (of which she has not), paraspinal muscle spasm, sciatic notch tenderness. MRI of the lumbar spine shows L4-5 and L5-S1 disc protrusion.
         1. What is the relationship of the fall to the neurologic findings?
         2. What diagnostic test should be done next?
         3. What might you expect to find if you examined the patient's parents?
         4. What would you expect the natural history of the back pain to be?


A 37 year old man develops polydipsia and polyuria. Lab studies confirm the diagnosis of diabetes mellitus and treatment with oral hypoglycemic agents is started. Two months later he complains of an uncomfortable burning sensation in the soles of his feet, worse at night and not present when he walks. The neurologic exam reveals absent vibratory sense in the toes and reduced at the ankles, reduced pinprick and temperature sensation in the feet, absent ankle reflexes, and absent response to stimulation of the sole and a normal motor exam.
         1. These clinical findings are best explained by what abnormality?
         2. Describe the different components of this neural structure and state the location of the lesion.
         3. What is the initial neurodiagnostic study indicated?
         4. Is the clinical history in this patient usual and characteristic?
         5. If parasthesias occurred most commonly when walking or alternatively when standing, would this raise alternative diagnoses?
         6. If you were asked to give an lecture on the neurologic complications of diabetes, what topics would you be sure to cover?


An 18 year old has been weak since childhod, has never been able to walk normally and has been convined to a wheelchair for 2 years.As a child he could not run or climb stairs or arise from a chair without using his hands to push off. A maternal uncle died at age 20 of progressive neurological illness, but the parents are normal. He has no siblings.

The neurologic exam reveals scoliosis, winging of the scapula, flexion contractures of the ankles, knees and hips. There is marked muscle weakness in the arms and legs (proximal greater than distal) and marked wasted, except for the calves, where bulk is preserved. Reflexes are present only in the ankles and triceps. The cranial nerves are normal.

CPK=3,000. EMG reveals myopathic potentials. Nerve conduction velocities are normal. A muscle biopsy reveals muscle atrophy with fat and conective tissue replacing muscle; dystrophin is shown to be absent by special staining.
         1. What type of myopathy does the patient have?
         2. What would genetic studies show?
         3. Can muscle weakness be avoided?


Harriet is an 18 year college freshman who develops abdominal pain and vomiting followed by diarrhea the next day, and a dry mouth. One day later she develops droopy eyelids, diplopia and difficulty standing and difficulty lifting heavy objects.

The neurologic exam reveals ptosis, bilateral facial weakness, pupils are 5mm and poorly reactive, reflexes are absent, and proximal greater then distal weakness. The sensory exam is normal. A chest film reveals a left lower lobe pneumonia; an abdominal film reveals colonic distention.
         1. What neuro impairments might cause these findings?
         2. Is a tensilon test warranted?
         3. What might electromyography/nerve conduction studies show?
         4. What therapy should be initiated?
         5. What is the difference between nicotinic and muscarinic receptor?
         6. Are these findings consistent with myasthenia gravis?
         7. Define fatigue.
         8. What tests are warranted in the patient suspected of having myasthenia gravis?


A 33 year old woman complains of blurred vision in her left eye and pain in the left orbital region (as if she had sand in her eye) especially when she moves her eyes. She has no headache, double vision, facial parasthesieas, or numbness. She has recently felt fatigued enough that she has started working part-time rather than full-time, has had multiple urinary tract infections and urinary frequency with nocturia. She complains that her legs become stiff when she walks long distances.

Visual acuity in the left eye is 20/70, in the right eye 20/20. The fundi are normal. There is a left centro-cecal scotoma. The left pupil does not react when light is shone into it; when light is shone into the right pupil both pupils contract, and when you swing the light in front of the left it dilates (afferent pupillary defect). The patient is generally hyperreflexic with plantar responses. Abdominal reflexes are intact and present; sensory and cerebellar exam are normal.
         1. Where's the lesion?
         2. What is the differential diagnosis?
         3. What diagnostic studies should be done?
         4. What are the treatment options?
         5. What is the natural history of this condition?


A 50 year old alcoholic stops drinking due to severe abdominal pain. That day he has a generalized seizure and is admitted to the hospital. He is confused, ataxic and reports double vision. His T-shirt reads "Rehab is for Quitters." Treatment with Ativan (lorazepam), Librium (chlordiazepoxide) and phenobarbital is instituted. He becomes increasingly lethargic and then obtunded.

The physical exam reveals icteric sclerae, multiple spider angiomas and an enlarged and tender liver. The neurologic exam reveals a lethargic mental status. There is *asterixis* no pronator drift and normal strength. He is generally hyperreflexic with bilateral extensor plantar responses. The sensory exam is normal. Cranial nerve exam reveals horizontal and vertical nystagmus and a left lateral rectus palsy. The fundi are normal.

Pertinent laboratory data (from the chem everything sent by the ER) includes an elevated bilirubin and alkaline phosphatase, a normal blood glucose, WBC 6000 and Hgb 12.1.
         1. Based on the clinical history and exam findings: Explain the mechanism of the neurological and medical disorder.
         2. What additional diagnostic studies should be done?


A 22 year old man whose roommate has recently died of AIDS becomes very depresed and suicidal. He injects himself with a blood of another HIV(+) friend so that they can "bond." Four weeks later he develops sore throat, fever, arthralgias and lymph node swellings. He then develops facial weakness, neck muscle weakness and shoulder weakness.

The neurologic exam reveals weakness of the entire face bilaterally, neck and proximal arm weakness, absent biceps and triceps reflexes. The CSF is acellular and has an elevated protein. Nerve conduction velocities are markedly slowed and electromyography shows normal muscle potentials.
         1. What has happened to this patient?
         2. What is the appropriate treatment?
After complete recovery he reports that his memory is poor and his thinking is slowed. He can not concentrate or sustain attention. He has difficulty sleeping and poor appetite. Neurologic exam reveals a Mini Mental Status Exam score of 27/30, but is otherwise normal.
         1. What is wrong with this patient?
         2. He is HIV (+). Is this AIDS dementia complex?
         3. What are some of the neurologic complications of HIV?


A 28 year old male with polysubstance abuse (cocaine, heroin, PCP) develops headache and muscle pain. He reports night sweats and loss of appetite due to difficulty swallowing. Two days later he reports back, abdominal and jaw stiffness. The past history is relevant for bacterial endocarditis treated with IV antibiotics 3 years ago and chronic schizophrenia treated with stelazine, haloperidol and clozapine, but the patient is usually non-compliant with these medications.

BP 200/100, HR 120, RR 22, temp 101. The neurologic exam reveals an alert, attentive man. His gait is stiff and antalgesic. Truncal rigidity is present but motor strength is normal. The reflexes are brisk and symmetrical, with bilateral plantar responses. Sensation is normal. The cranial nerves reveals orofacial dyskinesias with facial and jaw spasms and nuchal rigidity. There are multiple wounds. Laboratory studies reveals WBC 18,000 with a left shift, normal thyroid studies, CPK 2000, urine negative for myoglobin. A CT done by the ER is normal, and an LP done in the ER on RANDO criteria (Resident Ain't Never Done One) is normal as well. ECG reveals sinus tachycardia only. An EEG is normal.

The ER initially consults psychiatry for effect of antipsychotics, but he goes to medicine to be "medically cleared." Neurology is consulted when the patient becomes confused and develops generalized myoclonic jerks (described to you as seizure activity by the medicine resident). Respiratory stridor develops, the blood pressure rises to 220/130 and cardiac arrythmias develop.
         1. What is the differential, and what is the diagnosis?
         2. What clues were missed?
         3. What is the likely course and prognosis?


A 26 year old obese woman develops headache, double vision and a discharge from her left breast. Her last menstrual cycle occurred one year ago. She feels tired all the time and reports that her hair is falling out. The neurologic exam reveals a left lateral rectus paresis, decreased sensation on the left side of the uper face. The visual fields are full and the fundi are normal with spontaneous venous pulsations. The pupils are equal in size and react normally to accomodation and light.
         1. Where's the lesion?
         2. What diagnostic studies are indicated?
         3. What imaging should be performed?
         4. What is the appropriate treatment?


Six months following trans-sphenoidal hypophysectomy for a prolactin-secreting macroadenoma, headache and double vision recur. The headache is bi-frontal, episodic, increases with cough or sneezing and awakens her from sleep. Diplopia is horizontal and is maximal on far gaze. Neurologic exam now reveals a right lateral rectus paresis; the fundi are without spontaneous venous pulsations and there is blurring of the disc margins with centrally located hemorrhages and exudates. Visual acuity is 20/50 in the left eye with reduced perception of color in the left eye; the right eye is normal.
         1. What is the most likely explanation?
         2. What would skull roentgenogram, CT or MRI be expected to show?
         3. Is an LP indicated or contraindicated? What might it show?
         4. What is the treatment of this condition?
         5. If medical treatment fails, is there a surgical option? (Prospective surgeons note: there is not always a surgical option.)
         6. What is the major threat in this condition?


A 32 year old woman has difficulty understanding what people are saying in telephone conversations and in noisy crowded rooms. This is a major problem when she holds the phone to the right ear. She also notes intermittent slurring of speech and right facial numbness. The neurologic exam reveals decreased hearing in the right ear, mild right nasolabial flattening, an unsteady tandem gait, a decreased corneal reflex on the right. Using a 512Hz tuning fork, hearing is depressed on the right and air conduction persists when bone conduction terminates. Audiology reveals a high frequency loss on the right and impaired speech discrimination, and decreased brain stem auditory evoked potential on the right. Response to caloric testing on the right is decreased.
         1. What conditions should be considered?
         2. Where's the lesion?
         3. What would CT/MRI be expected to show?
         4. Why is a skin exam important?
         5. How would this lesion be treated?
         6. What neural structures might be injured?


A 52 year old legal secretary complains of right wrist pain. This is worse with activity and recurs at night. She has difficulty writing and using tools, and says she can not work due to tingling numbness in the fingers. Neurologic exam shows:
          o weakness of thumb flexion
          o reduced sensation over thumb and index fingers
          o absent ankle jerks bilaterally
          o reduced strength extending toes
          o positive Tinel and Phalen signs bilaterally
         1. Questions What neurological condition explains the findings?
         2. What might EMG show?
         3. What treatment might be suggested?
         4. What might neurontin or amitriptyline do?
While driving to work she is struck by the car behind her. Her head hits the steering wheel. The next day she has neck stiffness and soreness. Physical exam shows:
          o Neck exam shows straightening of the cervical lordosis and cervical paraspinal muscle spasm
          o Increased weakness of thumb flexion
          o triceps weakness
          o absent triceps reflex
          o reduced sensation in thumb, index and middle fingers bilaterally
         1. What is the mechanism of the new neurological dysfunction
         2. What is whiplash?
         3. What tests should be done?


A 10 year old boy falls on the ice and breaks his left radius and ulna. He is treated with a cast for 6 weeks. Following removal of the cast, he reports difficulty opening jars and cans.
          o Neurologic exam shows weakness of wrist flexion and finger adduction
          o reduced sensation of fifth finger and ulnar portion of fourth finger
          o normal reflexes
          o What is the cause of neural dysfunction?
          o What tests should be done?


A 40 year old homeless alcoholic sleeps on a park bench. When he awakens he has no use of his right hand. He has no headache, visual symptoms, numbness or difficulty walking.
          o Neurologic exam shows: weakness of wrist extension
          o marked weakness of hand and thumb
          o intact biceps and triceps reflex
          o normal sensation
         1. What has happened to this patient?
         2. What diagnostic studies should be performed?
         3. The ER has already performed performed a head CT and offers to write the orders for carotid dopplers, an echo and hypercoagulable state labs, and the nurse is calling for a bed. Is this helpful?


An 18 year old Tulane co-ed leaves for Florida by car on spring break. One week previously she started on an oral contraceptive pill. While sleeping in the back seat her friends report that she has frequent muscle jerks. In Florida she has generalized seizure activity after drinking a six pack of Miller Lite, and is dazed and confused for the next two hours.
          o On physical exam temp 98.4F, BP 110/80, HR 70 and RR a suspiciously normal 20
          o neck supple
          o head without trauma
          o a detailed neurologic exam is normal
          o Lab data WBC 10, 75% segs, 15% bands, 10% lymphs
          o CK 300
          o prolactin 100
          o Computed tomography normal (your read)
          o EEG multifocal spikes
         1. What is the diagnosis?
         2. What should her management be?
         3. Classify the epileptic event.
         4. Name factors which may trigger seizures?
         5. Is Miller Lite less filling, or does it taste great?


The student from the previous question refuses to take any anti-epileptic drug. She has no futher seizures until the day of last final exam, which occurs after she stays up all night with the help of No-Doz, Ritalin (given to her by a friend diagnosed with ADHD) and lots of coffee.

Physical and neurologic exams are normal.

She is started on carbamazepine (Tegretol), 200 mg TID. She compliant with treatment and therapeutic blood levels. Eight months later she has an episode during which she feels dizzy, light headed, weak, falls to the ground and is briefly unconscious; there is no post-ictal confusion.
         1. What is the likely mechanism?
         2. What tests should be done?
         3. List major side effects of antiepileptic drugs.


An 18 year old college freshman is found apneic and pulseless in her boyfriend's room after attending a fraternity party after the Tulane-LSU football game. CPR is initiated by her boyfriend; pulse and blood pressure are noted when paramedics arrive but she requires assisted ventilation. She is stabilized.
         1. Exam reveals Coma
         2. No spontaneous respirations
         3. absent eye movements
         4. no response to noxious stimuli
         5. Reflexes are 2+ and symmetrical with plantar responses
The next day respirations are spontaneous, pupils are reactive but she remains comatose. One week later her eyes are open but she shows no response to verbal stimulus. Eyes rove spontaneously but she does not follow objects in her environment and she has no reponse to auditory stimulus. She has limb movement to noxious stimulus but no voluntary movements; she continues to require ventilatory support. CT and MRI are normal, EEG shows low voltage theta waves.
         1. What happened to her?
         2. Define chronic vegetative state


A 35 year old supervisor of a nuclear energy plant begins to have episodes of falling asleep on the job. These occur at work and while driving. (Feel free to hum the theme from 'the Simpsons' now.) He has multiple near miss accidents and begins to ahve his friends drive him. After the episodes of excessive daytime sleepiness (each lasting 5 to 10 minutes)he feels better, more alert and refreshed. He is very concerned because these attacks are increasing in frequency and now occur multiple times daily. Also, he reports that when he laughts he feels weak an doccasionally falls to the ground. Family history is relevant that his mother and brother have epilepsy. Neurologic exam is normal.
         1. Questions What's the diagnosis?
         2. What would a sleep study show?
         3. What is a multiple sleep latency study?
         4. Deliniate the narcolepsy triad
         5. What is the appropriate treatment of this condition?


A 28 year old man slips and falls on his buttock. He complains of low back pain which persists despite bed rest and treatment with naproxen (an NSAID), carisoprodol (Soma, a muscle relaxant), and tramadol (Ultram, a serotonergic pain reliever).
          o Physical exam Normal lumbar lordosis
          o paraspinal muscle spasm
          o right sciatic notch tenderness
          o no pain on passive raising of the leg
          o detailed neurologic exam is normal
The pain persist and interferes with sleep. Amitriptyline is started in addition to other medications. One week later he has a generalized seizure. At this time, neurologic exam and EEG are normal.
         1. What is the likely mechanism of the seizure?
         2. What diagnostic tests should be done?
         3. What should his subsequent management be?


Sally is a 35 year old woman who has a history of sinus headache. She has strongly positive family history of headache. She had motion sickness as a child. At menarche, she develops episodic left temporal throbbing headache associated with nausea, photophobia and worsened by activity. Her headache responds to sumatriptan and occurs once per month. One decade later, she develops chronic daily heacache which is aching in type, associated with neck pain. She becomes increasingly depressed and anxious.

One night after 6 days of headache severe enough cause her to miss work, she goes to the ER with her bag of 23 different medications including hydromorphone (Dilaudid) and codeine/aspirin (Percodan) for a second opinion (yours).
         1. Classify her headache pattern.
         2. What treatment is appropriate?
         3. Is she an addict by the use of daily narcotics?



A 20 year old college student has an accident when an ice sculpture strikes her in the left frontal region. She has no loss of consciousness or amnesia for the event. She has mild headache and heck pain which resolves spontaneously. Three months later she has an episode of right facial twitching followed by generalized tonic-clonic activity, incontinence and post-ictal confusion.
          o Neurologic exam shows a R pronator drift
          o R hyper-reflexia and Babinski
          o EEG shows L frontal spike discharges
          o CT shows a L porencephalic cyst
         1. What is the mechanism of her episode?
         2. What is the nature of the episode?
         3. What is the relationship of trauma to the cyst and episode?


There's a 25 year old nurse in the ER nobody likes very much. We'll call her Mary. (Actually, everybody calls her 'that bitch,' but we'll be nice and call her Mary too.) One day she develops a severe occipital headache after an altercation with a colleague. The pain is intense and very uncomfortable, and after trying Aspirin and Tylenol without relief she goes to you for help. She has no prior headache history, and no history of headache in her family.

The neurologic exam is normal, as is a computed tomogram of the head.
         1. What is the diffential diagnosis?
         2. Should an LP be done?, other than the fact that you don't like her either?
         3. What are the risks of LP?
         4. What treatment is warranted?


Randy is HIV positive and takes highly active anti-retroviral therapy. He has a normal CD4 count and an undetectable viral load. He has no fatigue or weight loss. He reports new onset heacache, bitemporally, throbbing in nature, building up over 6 hours and ssociated with nausea.
          o On exam Neurologic exam is normal
          o Neck is supple and he is afebrile
          o CBC and chem everything are normal
         1. What's the differential diagnosis?
         2. What is the appropriate management?
         3. On LP you find
                o Opening pressure 18 cm H2O (normal)
                o 30 lymphocytes
                o protein 80 mg/dl
                o glucose 70 mg/dl
                o serology cultures and stains are normal
            What is the explanation for these findings?
         4. What are alternative explanations?



Sam is a 67 year old retired CPA. He develops left temporal aching pain and visual blurring. He has myalgias and pain on chewing food.
          o Neurologic exam shows left temporal artery tenderness
          o biceps muscle tenderness
          o left optic atrophy
          o when you shine a light in the R eye the L pupil constricts, but when you shine the light in the L eye it gets bigger again (afferent pupillary defect)
          o visual acuity 20/100 on the L
         1. What is the mostly likely diagnosis?
         2. What tests should be done?
         3. Suppose a temporal artery biopsy is normal. What next?



Immediately following delivery of her third child, Mary develops severe headache, diplopia and left eye blurring.
          o On exam BP 95/50, taken by you with a manual cuff and HR 110
          o L optic atrophy and afferent pupillary defect
          o bitemporal hemianopia
          o left lateral rectus (VI) palsy
          o left ophthalmic branch of trigeminal nerve hypoaesthesia
          o nuchal rigidity
         1. Is this eclampsia?
         2. Where's the lesion?
         3. What's the diagnostic study?
         4. What is appropriate management?
         5. What is the clinical significance of nuchal rigidity?


Harry is a 52 year old math teacher. He has hypertension and hypercholesteremia. Medications include Accupril (an ACE inhibitor) and pravastatin (Pravachol). One morning he awakens with L eye visual blurring as if a shade has been pulled down; he closes the L eye and his vision is normal in about 15 minutes. He then develops left sided aching neck pain which resolves with over-the-counter analgesics. He calls his physician, who makes a diagnosis of "ocular migraine" over the phone and tells him to make a routine appointment in 10 days for a checkup. His wife is not pleased with this advice and insists he see a neurologist (i.e. you).
          o On exam bilateral carotid bruits
          o L Hollenhorst plaque in retina
          o L superior temporal visual defect
          o normal pupillary response and acuity

         1. What's the diagnosis?
         2. What is the appropriate management?
         3. What vessels are involved?
         4. Why is this not migraine or cluster headache?
         5. Why is the pupillary response normal?


A 23 year old woman develops episodic headache lasting 30 minutes associated with diplopia on far gaze while driving. She has 6 episodes daily and they do not respond to medication. Other medications include tetracyclinc and tri-orthocycline for acne. She has gained 40 pounds in the past year.
          o Neurologic exam shows absence of venous pulsations and disc elevation in the eye
          o left lateral rectus paresis
          o bilateral enlargement of blind spots
         1. Explain the fundus findings
         2. outline a management strategy
         3. Should an LP be done?
         4. What are potention etiologies?
         5. The patient develops intermittent visual obscurations lasting ten minutes and intermittent pulsatile tinnitus. What is the significance of this?


An 8 year old boy develops intermittent headache and falls when running. He has intermittent horizontal diplopia when watching TV.
          o Neurologic exam shows broad based ataxic gait, falling to left
          o fundoscopy shows loss of venous pulsations
          o bilateral lateral rectus paresis
          o left sided dysmetria
         1. Where's the lesion?
         2. What are potention pathologic processes?
         3. What studies should be done?
         4. He suddenly vomits and becomes dazed, his respirations become labored, pulse slows and blood pressure becomes elevated. What has happened?
         5. What management is appropriate now?


A 24 year old man has 3 generalized major motor seizures. He has preceeding aura. EEG shows frequent bilateral symmetrical spikes. Treatment is intiated with depakote and he becomes seizure free. One year later, EEG is normal. Neuro exam and CT are both normal. Question:
         1. Patient asks "can I now drive"?
         2. "Do I need to continue medication"?
         3. Assume you permit him to drive and he drives 100 miles per day and he has an accident 3 years later but has no seizure related to the accident and medication does not make him drowsy. Despite this you and MD are named as a defendant in law suit because "patients with epilepsy should not drive". Defend your decision!


A 26 year old female graduate student was conducting a philosophy seminar when she suddenly started stuttering and then became incoherent. She seemed confused, and her mouth was twisted. One arm hung limply and she walked unsteadily. She had a past history of theumatic heart disease and took no meds except for birth control pills.
         1. What type of neurologic problem is this?
         2. Where's the lesion?
         3. What is the arterial supply?
         4. What is the most likely etiology?


A 68 year white female presents complaining of inability to walk. Upon further questioning you find that this has progressed over a month or two and is not associated with back pain. On exam she is slightly inattentive and sometiems inappropriate. Language is intact. She has no cranail nerve deficits, and good strength in the upper extremities. Her legs are diffusely weak, 3-4 of 5, proximally and distally. Sensory exam reveals questionable mild loss of light touch and pinprick distally over the legs, without a level. Reflexes are brisk in the legs and a Babinski sign is present bilaterally.
         1. Where's the lesion?
         2. What is the pathophysiology?


A 55 year old black female with a history of diabetes and hypertension states that while drinking her morning coffee she suddenly experienced "heviness" of the right arm. She fumbled with her cup until she spilled the coffee, and when the symptoms did not resolve within half an hour she came to the ER. Examination reveals an alert woman with normal mental status, and decreased light touch, pinprick, vibratory sense over the right arm and leg. Strength is normal.
         1. Where's the lesion?
         2. What is the vascular supply?
         3. What is the pathophysiology?
         4. You complete your evaluation 2 hours and 30 minutes after the onset of symptoms, and a chem everything, CT head, CBC, PT/PTT are all normal. The ER resident is extremely excited and is holding a      bottle of recombinant Tissue Plasminogen Activator (Alteplase) in his hands. Should you give it?


While working out at Reily uptown with free weights, your friend complains of sudden back pain and inability to walk. Your exam shows bilateral leg weakness, absent ankle reflexes (assume you have a reflex hammer in your gym bag), and decreased tone in the legs. He feels parasthesias running down the back of both legs, and doesn't notice you sticking his skin with a clean pin until the mid-thigh. Pressure on the lumbar spine is painful, and there is paralumbar muscle spasm.
         1. What happened?
         2. Where's the lesion?
         3. Is this upper or lower motor neuron?


A 35 year old black male is seen in clinic with a 3 month history of weakness and muscle cramps, first felt in the left arm but progressing to both legs. His voice is not as loud as it used to be, and is a little horse. Sometimes food gets "stuck" on one side of his mouth and he has to move it with his finger. He has no sensory loss. Reflexes are brisk, including a jaw jerk. The toes are equivocal. Fasciculations are present in the tongue at rest, and in all four proximal extremities. He is lost to follow up, but returns a year later complaining of trouble swallowing, shortness of breath and appears emaciated.
         1. Where's the lesion?
         2. What has happened in the time he was lost to follow up?
         3. Was it a particularly big mistake for the patient not to return?
         4. What will you do now?


A 62 year old woman complains of painand numbness of the hand. She has been dropping objects from the hand, but the discomfort is worse at night.
         1. What further history would help you localize the lesion?
         2. How can you tell mononeuropathy from myelopathy from diffuse peripheral neuropathy?
On examination you also find a loss of pinprick at the toes, and vibrations with a 128 Hz fork are felt for 10-5 seconds at the toes.
         1. What do you suspect now?
         2. What other findings might be present?


A 26 year old woman is referred to you by her psychiatrist. For the last year she has complained of weakness which came on after the death of her father. The weakness seems to come and go depending on her family situation and her depression. She also complains of a vague tightness of throat (?globus hystericus), leg aching and frequent headaches. Sometimes she is fine, and other times she just lays on the couch, or will suddenly fall walking off a curb. She admits she doesn't know how to "pull herself out of this."
         1. How will you proceed?
         2. Where's the lesion?
         3. What is causing her headaches and lump in the throat?


A 30 year old white female has difficulty climbing stairs. She cannot lift objects but has no problems writing or buttoning her shirt. Her gait is waddling. She has been followed for 8 months in rheumatology clinic for "arthritis" not otherwise specified, and a visit to the walk-in clinic prompted her appointment with neurology. The joints seem normal to your exam, but the thigh muscles are tender to palpation?
         1. Where's the lesion?
         2. What will be your lab workup?


A 28 year old white female complains of headaches for one year, recently daily. They are often throbbing, usually bitemporal and do not usually cause too much nausea, although she has vomited once or twice. She also says her vision has changed, but she went to get her glasses checked and was told they were fine. Other pertinent history is obtained that she had a child 9 months ago and gained 80 pounds during the pregnancy, of which she has lost 30.

On physical exam, she is obese. Vital signs are normal. Funduscopic exam shows bilateral disc margin blurring with a flame hemorrhage on the right. Pupils are equally reactive, and visual fields are full to confrontation. There is a question of mild lateral rectus weakness on the right. The remainer of the cranial nerve exam is normal, as is stength, sensation and reflexes, and gait.

      CT of the head is normal, as is an EEG. On lumbar puncture, the opening pressure is 41 cm H20.
         1. What is this syndrome?
         2. What severe disability is she at risk for?
         3. What would visual field testing be likely to show?

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