Itchy Skin

Inspired by last Friday’s AMR case, I thought I’d write an overview of the causes of pruritus, particularly the causes that DON”T go along with a rash (because I hate rashes? Nah).  You can organize these causes in a few ways, but I like to think of them based on the big categories of: dermatologic, systemic disease, neurologic, and psychogenic.

Only takes a few of these guys to set off some serious itching


Most dermatologic etiologies are going to have an associated rash, but it may be subtle. Here are a few where you make have to look closely:

  • Xerosis: The most common cause of generalized pruritus, just plain old dry skin. Common in winter, often can tell skin is try just by feeling it.
  • Scabies: Regular scabies, not the Norwegian kind discussed in AMR, may not have much of a rash associated. Sometimes you can see a burrow, but rarely. I learned that the itching is a delayed hypersensitivity reaction, and may not appear for weeks after infestation.
  • Atopic Dermatitis: Think of this in a patient with other allergic phenomena (rhinitis, conjunctivitis), sx at an early age, and a family history of allergic disease. Patients also have allokinesis, when an innocuous stimuli, like temperature changes or clothing, induces itching.
  • Contact dermatitis: there are two kinds of contact dermatitis. Irritant contact dermatitis (like that caused by poison ivy) occurs when an irritant directly damages the skin.  There is often a rash in this instant.  Allergic contact dermatitis occurs when the irritant induces an allergic response. The rash here may be diffuse and obvious, or may be more subtle. Ask about anything that comes in contact with skin, including soaps, lotions, and laundry detergent.

Systemic Disease

  • Cholestasis: The first thing we think of, but pretty rare. Most commonly starts in the palms and soles before becoming more generalized. Disorders that cause cholestasis include: Primary biliary cirrhosis, cholestasis of pregnancy, viral hepatitis, and anything that causes obstructive jaundice.
  • Renal disease: We think about this in uremia, but it is actually common even in dialyzed patients. Worse at night or after a dialysis session,
  • Malignancy/hematologic disorders: More often with hematologic malignancies than with solid tumors. Think of: Hodgkin’s disease, Polycythemia vera (worse in water), Carcinoid (thank you, histamine), and cutaneous T cell lymphoma. Patients without a diagnosis for their pruritus may be at increased risk for malignancy.
  • Thyrotoxicosis: cause you can’t have a list without thyroid on it. Actually, a fairly common sx of Graves disease.  hypothyroidism can cause xerosis, which itches
  • Connective Tissue Disease: Common with dermatomyositis and scleroderma in particular.

Brachioradial pruritus


Small fiber neuropathy may be associated with pruritus, so anything that causes neuropathy could lead to itching, including diabetes.  These are typically localized to the affected area, however.

  • Post herpetic neuralgia: Up to 50% of patients with post herpetic neuralgia experience this as itching rather than pain.
  • Notalgia Paresthetica: Itching on the upper back, perhaps due to trapped nerve fibers in the T2-T6 nerve roots. Unilateral, near the medial or upper border of the scapula.
  • Brachioradial pruritis: Itching of the proximal dorsolateral forearm, but may extend up to the upper arm or even trunk. Feels better with ice application. Similar to notalgia paresthetica, this may be related to nerve root entrapment in C5-C8, but also may have something to do with sun exposure.
  • MS: Compared to the rest on this list, MS is more likely to cause generalized pruritus. Typically a relapsing, remitting type course that mirrors the rest of the disease.


  • Psychogenic excoriation: Skin is normal, but affected individuals pick and scratch at it. Lesions are all within reach of the patient, and may be precipitated by psychologic stressors.
  • Delusional parasitosis: Patients experience a firm, fixed belief that they are infested by parasites, despite a lack of evidence of infestation.  This may be secondary to another psychiatric disorder, or may be the primary disorder itself.
  • No matter the underlying etiology, pruritus may get worse under emotional stress.

For many, the itching itself causes emotional stress. It impacts sleep, work, relationships. Relief can really improve your patient’s quality of life, plus you may uncover a systemic disease earlier.

If you are itching after reading this post, that is probably psychogenic itching. Good luck!



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!


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.