Neuro Cases Flashcards
63 year old male presents to clinic with a 15 year history of a gradually progressing tremor in both of his hands, with decreasing balance. Sometimes his voice also seems to have a tremor as well. His brother and mother have both experienced similar symptoms. The tremor is worse with fine distal movements. He notices that it tends to improve after dinner, once he’s had a beer for the night. What exam findings do you expect, what is your differential diagnosis, and how will you treat the most likely cause?
DDx: essential tremor vs kinetic tremor vs Parkinson disease
This is essential tremor. Begins gradually, immediate tremor, no other neurological deficits. Half of cases are autosomal dominant within families. May improve with low doses of alcohol. Caused by increased thalamic activity.
Kinetic/intention tremor would be from neocerebellum output disruption in MS or from red nucleus output disruption in trauma.
PD would have other neurologic deficits (stooped, shuffling, slow, other speech probs, anosmia, memory issues), tremor appears at rest and appears slowly.
Exam findings: cogwheel effect WITHOUT rigidity, tremor is ratchety and about 8 Hz, no other focal neuro deficits
Tx: beta blockers (propranolol) in younger patients, avoid if asthma, DM, other contraindications to beta blockade
Anti seizure meds like primidone can help, but may cause drowsiness.
Severe cases may require surgery or deep brain stimulation.
37 year old F presents to clinic with frequent recurring headaches that she describes as pounding and pulsatile, usually on the left, that sometimes make her nauseous and light-sensitive. She has a sister with similar symptoms. You review her medication list in the chart before going in to do an exam. She takes butalbital for headaches (prescribed by her old PCP in her previous hometown), an estrogen-progesterone oral contraceptive, cetirizine for allergies, and naproxen for headache and occasional back pain. When you obtain a social history, she endorses daily caffeine use, daily exercise, and occasional alcohol use. She denies tobacco or illicit drugs. Based on this, what is your diagnosis for her headaches, and what lifestyle modifications may help?
Migraine headaches: characterized by pounding, pulsatile pain, unilateral pain, worse with activity, often with nausea/vomiting/photophobia/phonophobia. About 20% of patients will have aura. Family history is common.
Medication overuse headaches can occur from frequent use of headache meds, especially butalbital, but also occasionally NSAIDs. Headaches can also occur with multiple other meds - beta blockers, nitrates, indomethacin, PDE inhibitors. Estrogen use can worsen migraines. Caffeine use can also worsen headaches.
Discuss with this patient: a better headache medicine regimen (probably avoid the butalbital), limit caffeine and alcohol, consider switching to a contraceptive that does not contain estrogen.
Acute treatment with triptans, prevention with propranolol and amitriptyline.
You are following a patient who has a history of migraine. She has previously taken 1000 mg acetaminophen for her headaches, but finds that it does not provide enough relief, and doesn’t do anything for her associated severe nausea. Recommend a regimen for treatment and prevention of her migraines.
Treatment: try sumatriptan for the migraine, with prochlorperazine (compazine) or metoclopramide (reglan) for the nausea.
Triptans are 5-hydroxytryptamine receptor agonists leading to cerebral vasoconstriction. May cause paresthesias, good idea to evaluate for cardiac risk factors first.
Prevention: propranolol, amitriptyline. May also use topiramate.
A 31 year old man is awakened in the middle of the night by a unilateral knife-like headache centered behind his right eye. He feels congested as well. He presents to the ED due to the sudden onset of symptoms. In the ED you see him pacing around the room, and he seems agitated. What red flag symptoms do you want to make sure you rule out, and once you have settled on the most likely diagnosis, what treatment/prevention do you recommend?
This is most likely a cluster headache: unilateral retroorbital sharp pain, can awaken the patient from sleep, patients may be congested, restless, agitated.
Red flags would be: worst headache of life or thunderclap headache (SAH), associated fever or stiff neck, behavioral changes, cancer history, first presentation of a headache with exertion, new headache type after age 50.
Treatment: high flow O2 given by face mask, sumatriptan for acute attacks. For prevention, verapamil.
An 82 year old male presents to the ED with chief complaint of confusion. Per his daughter, he has not been acting like himself over the past few days, and she reports that he wasn’t paying attention when she came to check on him this morning, and his speech was disorganized and rambling, unlike his usual coherent self. He does not have a history of dementia. What is going on? What additional history do you want to elicit? What physical exam findings do you want to check for? What labs/other tests do you want to order? Based on all of this, what is contributing to his condition?
Delirium… time to figure out the etiology. Patient has acute and fluctuating presentation with confusion and inattention, over a span of hours to days.
Additional history: His wife died about 6 months ago and he has been living alone since then. Things have been “up and down” in the daughter’s words. PMH of HFpEF and T2DM, meds include lisinopril, carvedilol, furosemide, hydrochlorothiazide, atorvastatin, metformin. He was just in the hospital three weeks ago with a CHF exacerbation, at which time his furosemide dose was increased from 40 mg daily to 80 mg daily.
Exam: appears appropriate for age, but speech is garbled and incoherent, he is inattentive, impaired concentration, and appears drowsy. Tachycardic, BP in the 110s/60s, normal respiration rate, sufficient O2 saturation. No signs of trauma. Mucous membranes appear dry, there is mild skin tenting. CV exam shows tachycardia and a 2/6 holosystolic murmur at the apex (previously documented). No JVD. Pulm exam CTAB. Abdominal exam benign. No focal defects on neuro exam.
Labs: UA shows bacteriuria without nitrites, WBCs, or leukocyte esterase. CBC is within normal limits. BMP shows hyponatremia and hypokalemia. Blood glucose is 125.
Possible contributors are volume depletion (in the setting of lasix plus hydrochlorothiazide), his recent med increase, his recent CHF exacerbation, loss of wife recently, possible UTI.
A 28 year old woman presents to outpatient clinic with an episode of weakness in her R foot causing her to trip frequently. On review of systems she denies back pain, bowel or bladder symptoms, headache, vision changes, and other episodes of weakness, although she does say that a little over one year ago, she presented to an urgent care center in another state with blurred vision and decreased perception of color, which resolved in a few days. What is your most likely diagnosis and why, and what tests will you do to make the diagnosis?
This is most likely multiple sclerosis, with lesions disseminated both in space and in time. MS is a disease process with focal demyelination within the brain and spinal cord. It is limited to the CNS. The demyelinating plaques that form are full of inflammatory cells, suggesting that this is an autoimmune disease. Demyelination of axons leads to their degeneration, causing a disease that is often progressive and disabling. Clinical presentation initially is frequently optic neuritis (blurred vision, decreased color perception), and other manifestations include trigeminal neuralgia, motor dysfunction like limb weakness or stiffness due to compromise of the corticospinal tract, sensory symptoms, cerebellum symptoms, Charcot’s triad (intention tremor, dysarthria, and nystagmus), facial myokymia (wormlike movement of facial muscles), vertigo, and sensations of electricity in the limbs (Lhermitte sign). Symptoms are often worsened by heat.
To diagnose: MRI with gadolinium contrast, looking for lesions that are bright on T2, and are linear or ovoid and often at right angles to the ventricles (Dawson’s fingers). Lesions larger than 5mm or infratentorial often help to confirm the diagnosis. FLAIR is also particularly good at detecting lesions. LP will also diagnose it, as patients with MS will frequently have CSF with elevated IgG and 2 or more oligoclonal bands and increased myelin basic protein. Oligoclonal bands are not specific to MS but they are pretty sensitive. MS, however, is a clinical diagnosis.
A 52 year old woman is brought into the ED after having a seizure. Prior to the seizure, per her husband, she complained of a severe headache, and vomited, then becoming more and more confused. Her right pupil is dilated and she has right ptosis. She does not withdraw to pain on the left side. She has a left facial droop. Her medical history is significant for hypertension. Per her husband, she does not have a history of headaches, except for one episode of headache following a jog about a week and a half ago. What is your immediate differential? What are the first few things you will do for this patient? What is most likely going on?
DDx: Subarachnoid hemorrhage vs ischemic stroke vs Todd’s paralysis
Most likely to be a SAH due to a) history of one previous headache about two weeks before following exercise, b) HTN, and c) “worst headache of my life”. Does not appear to localize particularly well as right pupil dilation/ptosis suggests a R side midbrain lesion, L facial droop and L weakness/sensory loss suggests a R cortical lesion, and vomiting suggests possible involvement of CN X in the medulla, or at the very least increased ICP.
1) ABCs! If GCS<8 or if patient is not protecting her airway, intubate. Establish vascular access.
2) Head CT non-contrast is the most sensitive imaging. Should show hyperdensity in cerebral convexities, cisterns, and parenchyma, potentially also in ventricles (worse prognosis). Can do LP later if head CT is negative looking for xanthochromia (yellowish CSF)
3) Intervene. Angiography to coil the ruptured saccular (berry) aneurysm is superior to clipping, but clipping can be done in the first 48 hours.
4) reduce vasospasm: use Hypertensive Hypervolemic Hemodilution as well as nimodipine (CCB)
5) Address other complications
You have a patient with polycystic kidney disease. What potential neurologic complication should you advise him about?
Cerebral aneurysm, most commonly in the anterior communicating artery, although multiple aneurysms can be seen.
You are following a patient who is on hospital day 5 following admission for subarachnoid hemorrhage. Yesterday she was able to answer all your questions without difficulty but today appears much less alert. What major complications are you concerned about?
Delayed vasospasm lethargy or acute hydrocephalus are both major complications that should be considered if the patient’s mental status worsens, and an emergent head CT should be performed to assess whether there is a need for angiography or ventriculostomy. Admittedly, transcranial doppler is better at detecting vasospasm, but CT is better in this emergent situation.
A 29 year old police officer presents to the ED with weakness on the right side following an altercation with a burglar in which the officer was temporarily placed in a choke hold. On exam her left pupil is 2mm and her right pupil is 4mm, she has left-sided ptosis, but pupillary light reflex is intact. What is the most likely diagnosis, and what imaging should you obtain?
Acute ischemic stroke following L carotid dissection. The pupillary findings are a Horner syndrome (ipsilateral ptosis and miosis). RFs include trauma, severe coughing/sneezing/vomiting, EDS, fibromuscular dysplasia, and Marfan syndrome.
Obtain a head CT noncontrast to evaluate and rule out acute bleed. When the infarct is seen, this patient should go get a cerebral arteriogram for appropriate stenting of the carotid dissection, which should be followed by anticoagulation.
A 40 year old woman presents to your neurosurgery clinic following emergent treatment of a subarachnoid hemorrhage. Angiogram performed at that time showed a “puff of smoke” appearance of vessels in the circle of Willis. What is this disorder called?
Moya Moya
