Tremors

Not my recommended diagnostic approach

No, not a post about obscure Reba McEntire and Kevin Bacon projects of the 1990s, but the rhythmic shaking movements  that may be seen in your patients.  Step one with any diagnostic dilemma, history and physical. First, describe the tremor.

  • Rest tremor: Occurs at rest, with affected body part fully supported, goes away with action. It gets worse with movement of another body part (repetitive moving of the unaffected arm) or with mental stress (ask patient to count backward).  You should think about Parkinson’s Disease in patients with rest tremor, although PD can present with action tremor as well.
  • Action tremors: Most tremors are in this category, which is subdivided further into postural, kinetic, or intention. The most commonly diagnosed action tremor is Essential Tremor, it can present with any of these subtypes.
    • Postural tremors get worse when maintaining a position against gravity.
    • Action tremors are worse when doing an activity, walking, writing, holding a cup, etc.
    • Intention tremors are action tremors that get worse at the end of the activity. This is the tremor that is worse as the patient gets closer to the target on a Finger-Nose-Finger test. Think about a cerebellar issue in a patient with this type of tremor.

Now that you have described the tremor, it is useful to think of the features of different tremor types to help you sort out the diagnosis.

Parkinsonism:  Classically a pill rolling, resting tremor of the hand, that starts unilaterally.  As with other rest tremors, it gets worse with movement of another body part.  This may mean that it seems to be exaggerated with movement, like walking, but if you look closely you notice that the tremor stops and starts again when the patient assumes a new rest position.  Look for other symptoms of PD: bradykinesia, postural instability, rigidity, shuffling gait, masked face.

Physiologic tremor.  Everyone experiences this, but it is generally complained about unless it becomes exaggerated with caffeine, medicines, fatigue, or stress. Physiologic tremor is low amplitude, high frequency tremor present at rest or with action, and comes and goes with exposure to above stressors. Commonly prescribed medicines that can exaggerate tremor include stimulants, steroids, tricyclic antidepressants, atorvastatin, and verapamil.

Essential Tremor: The most common pathologic tremor, it is classically a symmetric, postural action tremor of the hands and wrist, but it may involve head, voice, or lower extremities.  It is generally severe enough to impact daily life, and patients may quit working due to the tremor.  About 50% of patients will describe a family history, and then it may be called familial tremor.  There should be no other neurologic signs.  It may get better with alcohol, and doesn’t get worse with caffeine.

Cerebellar Tremor: Is a slow action tremor, usually an intention tremor, and is generally found with other neurologic signs like ataxia, dysmetria, and hypotonia.  Differential diagnosis includes multiple sclerosis, stroke, and brainstem disorders.

Psychogenic Tremor: And of course, there is a psychogenic tremor. It may have abrupt onset, spontaneous remission, and changing characteristics.  It tends to occur in patients with psychiatric disorders and other somatizations.

Check out this article for a great summary: Crawford P, Zimmerman E. Differentiation and Diagnosis of Tremor. Am Fam Physician. 2011;83(6)697-702.

This post inspired by an IM IV patient encounter. If you have clinical questions that you think should be shared, let me know and we’ll write a post together!

Diarrhea…Cha, Cha, Cha

Every year during baseball season, certain things just return to my consciousness.

Lucky you, this year I’ve turned this childhood favorite into a blog post!  It’s time to talk about chronic diarrhea (I know you are excited).  Much credit to Dr. Erin Contratto who prepared this topic for AMR last month, and from whom I’ve stolen a lot of this information. Here’s a case to get us started.

65 year old female who complains of 6 months of intermittent diarrhea. She has periods of up to 10-15 loose, watery stools a day, other times she has more like 2-3 stools.  She frequently wakes up at night with crampy abdominal pain and diarrhea.  She has tried to eliminate lactose and gluten for short periods during this time, but it didn’t really make a difference.  She has not seen any blood, has not had fevers, has not lost any weight.  She doesn’t have stools that are greasy or hard to flush. No one else at home has similar sx.  She lives in the city, doesn’t camp, and hasn’t traveled in this time.

She has diabetes that is currently diet controlled with an HbA1c around 6.5%, hypertension, and GERD. She has not had medicine changes.

Step 1 is to classify the diarrhea as Fatty, Inflammatory, or Watery.  Fatty diarrhea will be hard to flush, and patients may describe a greasy sheen on the water in the toilet.  Malabsorption is the most common diagnosis in this category. Inflammatory diarrhea is characterized by blood, fever, and abdominal pain, and may get you thinking about infection, ischemia, or inflammatory bowel disease (the i’s have it?).  Watery diarrhea is more common than either of the other types, and is just what it sounds like, voluminous watery stools- without blood or fat.

Step 2- Is the watery diarrhea osmotic or secretory?  I try to reason these out based on the wording.  Osmotic diarrhea refers to “something” in the colon that attracts/keeps water there- leading to more water in the stool/diarrhea.  Polyethylene glycol is an osmotic laxative so would cause an osmotic diarrhea.  The pathologic etiologies of osmotic diarrhea include factitious ingestion of these kinds of laxatives, as well as carbohydrate malabsorption.  Osmotic diarrhea often occurs after meals (after the ingestion), and thus doesn’t wake patients up at night.

Secretory diarrhea on the other hand, refers to something secreted into the colon that then leads to the diarrhea. This can occur any and all times of the day, and often wakes patients up from sleep.  Included in this category are: post-cholecystectomy syndrome (from bile salts), certain toxins, and, neuroendocrine tumors, and vasculitis.  Also here is colitis, particularly microscopic colitis, disordered motility (IBS, hyperthyroidism), and cancer. Based on history, our patient has secretory diarrhea.

You could also calculate a stool osmotic gap to figure out secretory vs osmotic. The formula is           290 – 2 ({Na+} + {K+}), and a gap >125mOsms suggests osmotic diarrhea, while a gap <50mOsms suggests secretory.

Step 3: Once you figure out the big category, you can run down a differential diagnosis and decide what testing to order.  Commonly done: hemoccult, stool WBC, c.diff toxin, serum and stool electrolytes, qualitative fecal fat, laxative testing.  Certainly you wouldn’t do everything on every patient, but use your history and physical as a guide.

Step 4: What about endoscopy?  Many patients with chronic diarrhea will end up getting either a colonoscopy or flex sig.  Certainly if there is weight loss, fever, bleeding/iron deficiency, or unclear diagnosis, you would consider. Patients with typical IBS signs and no red flags may not require endoscopy.  Flex sig may be fine for an initial test, but consider getting the full colonoscopy if you are concerned for Crohn’s disease (to look at terminal ileum), malignancy, or bleeding.

From here, you’ll treat the disorder that you uncover.  And that is a post for another day…

 

 

Vertigo

Well, I was publicly called out this week to do a post, so I better deliver. Thanks much for the suggestion,  my goal is always to provide interesting, relevent content that helps you out in clinic.  Remember that you can search the whole blog with the search box, tags, or use the big categories at the top of the page. Archives are there to help you!

Anyway… on to vertigo!

Vertigo is a sensation of movement without moving.  If you’ve done this…

or this…or this…

then you know vertigo.

A big branch point in the differential diagnosis is Central vs Peripheral causes. Central causes are the “scarier” ones: brainstem or cerebellar stroke/TIA or MS. Peripheral causes are the ones we are more comfortable diagnosing and treating: BPPV, Meniere’s diease, vestibular neuritis, acoustic neuroma. Migrainous vertigo can walk the line between central and peripheral, and have features of both.

Most vertigo has some postural instability associated, and it often feels worse to move the head in the midst of an attack. Specific, predictable maneuvers (like rolling over in bed) that precipitate vertigo should make you think of BPPV. Most patients with peripheral causes of vertigo should be able to walk. When the postural instability is so severe that they can’t walk, that points toward a central cause.

Vertigo doesn’t last forever. Even with permanent damage to the vestibular system, the body compensates and the vertigo subsides. However, the time course can help you with the diagnosis: BPPV usually is short-lived– a minute or less, while migrainous vertigo can last minutes to hours.  Vestibular neuritis, brainstem infarction and MS can produce vertigo that is severe and lasts for days.

Nystagmus is often found with vertigo. Central causes can have nystagmus in any direction, while peripheral causes will only have horizontal nystagmus. Nystagmus that reverse direction when the patient looks from right to left suggests a central cause.

Apart from the Romberg and nystagmus, an otherwise normal neurologic exam suggests a peripheral cause.  If your patient has weakness, cerebellar signs, or abnormal reflexes, be worried about those central causes.  Interestingly, hearing loss or tinnitus does suggest a peripheral cause, most commonly Meniere’s disease or acoustic neuroma.

Of course, there are some specific maneuvers that can help you out. The Dix Hallpike maneuver is most helpful if your patient is not symptomatic when you examine them. If you can elicit the vertigo and/or nystagmus with the maneuver, it is suggestive of BPPV.  My favorite video demonstration of Dix-Hallpike is here.

There is also the Head Thrust Maneuver. This is useful for diagnosing vestibular neuritis as compared to a central vertigo. The concept is that the patient focuses on a distant object, and tries to maintain focus while the examiner abruptly turns the patient’s head about 15 degrees. A normal response is to keep the eyes fixed on the object.  Patients with cerebellar lesions have a normal response. The abnormal response is for the eyes to deviate, toward the lesion, and then slowly return to the object. Peripheral causes of vertigo, like vestibular neuritis, tend to result in an abnormal head thrust response.

Up To Date has a great table to help differentiate the common and concerning causes of vertigo. It is so good, I’ve just reproduced it here for you.  Another great resource for dizziness in general is this AAFP article (if you don’t have institutional access, Am Fam Physician. 2010 Aug 15;82(4):361-368).
Time course Suggestive clinical setting Characteristics of nystagmus• Associated neurologic symptoms Auditory symptoms Other diagnostic features
Benign paroxysmal positional vertigo Recurrent, brief (seconds) Predictable head movements or positions precipitate symptoms Peripheral characteristics None None Dix-Hallpike maneuver shows characteristic findings
Vestibular neuritis Single episode, acute onset, lasts days Viral syndrome may accompany or precede vertigo Peripheral characteristics Falls toward side of lesion, no brainstem symptoms Usually none Head thrust test usually abnormal
Meniere disease Recurrent episodes, last minutes to several hours Spontaneous onset Peripheral characteristics None Episodes may be preceded by ear fullness/pain, accompanied by vertigo, unilateral hearing loss, tinnitus Audiometry shows unilateral low frequency sensorineural hearing loss
Migrainous vertigo Recurrent episodes, last several minutes to hours History of migraine Central or peripheral characteristics may be present Migraine headache and/or other migrainous symptoms accompanying or following vertigo Usually none Between episodes, tests are usually normal
Vertebrobasilar TIA Single or recurrent episodes lasting several minutes to hours Older patient, vascular risk factors, and or cervical trauma Central characteristics Usually other brainstem symptoms Usually none MRI w/DWI may demonstrate vascular lesion
Brainstem infarction Sudden onset, persistent symptoms over days to weeks As above Central characteristics Usually other brainstem symptoms, especially lateral medullary signs Usually none; an exception is anterior inferior cerebellar artery syndrome MRI will demonstrate lesion
Cerebellar infarction or hemorrhage Sudden onset, persistent symptoms over days to weeks Older patient, vascular risk factors, especially hypertension Central characteristics Gait impairment is prominent. Headache, limb dysmetria, dysphagia may occur. None Urgent MRI, CT will demonstrate lesion
* Other diagnoses described in text “Pathophysiology and differential diagnosis of vertigo”.
• Peripheral characteristics of nystagmus: horizontal or horizontal-torsional; suppresses with visual fixation, does not change direction with gaze. Central characteristics of nystagmus: may be horizontal, torsional, or vertical, does not suppress with visual fixation, may change direction with gaze.