What causes numbness and tingling?

Numbness and tingling is one of the most common reasons for a visit to the neurologist, and it is usually the pattern or distribution of the numbness that is the key to figuring out the diagnosis:

1. Numbness in the hands:
This is most often caused by carpal tunnel syndrome (CTS). CTS is caused by median nerve compression at the wrist(s), and will usually present with numbness and tingling in one or both hands, mostly affecting the thumb, index and middle fingers (but sometimes the whole hand), worse at night or with certain wrist positions like driving, typing or holding a book, and alleviated by vigorously shaking the hand. In severe cases, there can be weakness or wasting of the muscles at the base of the thumb. Most patients can be treated conservatively with a neutral position wrist splint, but severe or recalcitrant cases will require surgery.

Ulnar neuropathy at the elbow (funny bone) can also cause numbness and tingling in the hand, usually mostly affecting the ring and little fingers, worse at night or when leaning on the elbow. Severe cases can be associated with wasting of the muscles between the knuckles and clawing of the hand. Mild cases can be treated with an elbow pad, but severe cases will necessitate surgery to decompress or transpose (move) the nerve.

2. Numbness in one foot:
A plantar neuroma is caused by injury and scar tissue, and causes pain and numbness between the toes, worse with weight bearing and walking, and usually responds to a local injection, although occasionally needs surgical excision. Tarsal tunnel syndrome, sometimes thought of as the lower extremity equivalent of carpal tunnel syndrome, results from compression of the tibial nerve at the ankle, and causes pain and numbness in the sole of the foot, worse from standing and walking. Symptoms sometime improve with orthotics, but rarely necessitate surgical decompression. Numbness in one foot can occasionally be seen from lumbar radiculopathy,but then will be usually be associated with back pain and sciatica.

3. Numbness in both feet:
So called “glove and stocking” or length-dependent numbness indicates numbness, tingling, and (in some cases) burning pain in the distal extremities usually from axonal polyneuropathy. The diagnosis can be confirmed by electrodiagnostic testing and/or skin biopsy. The most common cause is diabetes. Treatment is aimed at the underlying process, such as controlling the blood glucose in diabetics, scrupulous foot care to prevent painless injuries, and medications for symptomatic treatment of neuropathic pain.

4. Numbness in one thigh:
This is usually from meralgia paresthetica, which results from compression of the lateral femoral cutaneous nerve in the groin, and causes numbness and burning pain the the lateral thigh. It can be triggered by weight gain, weight loss or tight fitting clothes, and usually resolved spontaneously, although recalcitrant cases can be treated with a nerve block.

5. Numbness in both legs:
Numbness in both legs that comes up on to the waste in a sensory level usually indicates spinal cord lesion, and can be of acute onset in transverse myelitis, spinal cord infarction or disc herniation, or more chronic onset from multiple sclerosis, spinal cord tumor, or vitamin deficiency.

6. Numbness that radiates down one arm or one leg
This is most likely radicular pain from a pinched nerve root in the neck or back.

Piriformis syndrome from compression of the sciatic nerve in the buttock is rare cause of “sciatica”, and is frequently misdiagnosed as radiculopathy. Affected patients complain of pain in the buttock that radiates down the back of the leg, made worse by sitting or wearing a wallet in the affected back pocket, and relieved by standing and walking. Many patients improve with therapy and exercise, but some require nerve blocks or decompressive surgery.

7. Numbness on one side:
Numbness that affects the face, arm and leg on the same side of the body usually indicates a brain lesion on the opposite side. Sudden onset one sided numbness can indicate a stroke. More gradual onset numbness on one side can indicate multiple sclerosis or a brain tumor. Affected patients will need to undergo a brain imaging study, and treatment will depend on the underlying cause.


Do you have a sleep disorder?


Excessive daytime sleepiness is often a symptom of an underlying sleep disorderClick here to take an on-line test to see how sleepy your are.


Obstructive Sleep Apnoea and Snoring
  • Sleep apnea is estimated to be prevalent in about 5% of the adult population.  It is characterized by partial or complete obstruction of the upper airway with continued respiratory effort.  As an individual sleeps, one’s upper airway may collapse, leading to interruptions in breathing known as apneas.  As these continue throughout the night, one has to wake up repeatedly to breathe normally.  These “micro-arousals” from sleep lead to a non-restful sleep period and sleepiness during the day.  The typical symptoms of sleep apnea are excessive daytime sleepiness, loud snoring, and having apneas that are witnessed by a bed partner.  Obesity is a predisposing risk factor.  Sleep apnea itself is a risk factor for uncontrollable hypertension, heart attack, and stroke.  It is treated by using a positive pressure breathing apparatuses that work as a “pneumatic stent” to prevent the airway from collapsing.


  • Insomnia is a highly complex sleep disorder that can manifest as excessive sleepiness.  Insomnia is very often secondary to other medical issues, other sleep disorders, or most commonly, stress and anxiety.  Obtaining a thorough medical history, including a discussion of stress and anxiety, is essential in the proper diagnosis and treatment of insomnia.

Restless Legs

  • Restless leg syndrome can prevent sleep, and therefore result in sleepiness during the day.  It is characterized by an urge or desire to move or kick legs while trying to fall asleep.  People who have this syndrome often need to get up and walk around to relieve this sensation.  It can be treated with a variety of medications.  Interestingly, iron deficiency can sometimes cause RLS and supplementation with iron in these people can often alleviate the symptoms.


  • Narcolepsy is a disorder of inappropriate intrusion of sleep into being awake.  It is typically diagnosed in individuals in their 20’s.  The popular misconception of narcolepsy is somewhat misleading.  Most people with narcolepsy have an unshakeable desire to sleep and often doze off in inappropriate settings.  However, most people do not simply collapse on the street, asleep – as popular depictions of narcolepsy suggest.  Narcolepsy is often accompanied by symptoms of sleep paralysis, a sensation of being paralyzed after waking up for about a minute, hallucinations when falling asleep or waking up, and cataplexy.  Cataplexy is a unique symptom of narcolepsy where individuals lose muscle tone when they are surprised.  It is somewhat rare, but is diagnostic of narcolepsy

The treatment of sleep disorders can markedly improve a patient’s quality of life as well as reduce cerebrovascular and cardiovascular risk.

A referral to a sleep specialist is highly recommended to evaluate for these disorders.

A polysomnogram is usually necessary to diagnose sleep disorders. The sleep lab is part of the hospital, but is an outpatient procedure during which we watch you sleep for the night.  There are electrodes attached to the head, next to the eyes, on the chin, and both legs.  There are also heart leads, a pulse oximeter, and a belt around the chest and abdomen to measure work of breathing.  Despite how it sounds, most patients fall asleep normally.

This post is provided courtesy of Dr Matthew J. Davis, Fellowship Trained Sleep Neurologist.

Jet Lag

This post is provided courtesy of K. T. Weber, Drexel University College of Medicine Class of 2013:

Most travelers are familiar with jet lag. Daytime sleepiness, difficulty focusing, uncoordination, digestive issues and immune system malfunctioning can all plague those who have ventured far from home. Nearly every travel website promises advice for curing jet lag – get outside in the sunshine, try to keep yourself awake, exercise in the evening and so on. But does any of the advice work? … and why?


Jet lag (“desynchronosis” or “circadian dysrhythmia”) is the result of moving rapidly through multiple time zones. It is caused by disruption of the body’s natural circadian rhythm, specifically the release of melatonin by the pineal gland in response to light and dark patterns. Traveling through more than five time zones shifts a person far enough off his or her normal activity cycle that waking and sleeping are affected. When sleep gets affected, concentration and cognitive performance quickly decline. Traveling west tends to have less jet lag, because it stretches the cycle out rather than shoving the circadian rhythm ahead in the light/dark pattern as traveling east does.


Melatonin is the link between the external environment and internal clock. It is released by the pineal gland, and light inhibits the release. Therefore it makes sense that melatonin, associated with dark, acts in favor of decreased activity and promoting sleep. Melatonin supplements (exogenous melatonin) is available from health food stores and a variety of non-prescription sources, and preliminary data suggests it decreases jet lag when taken shortly before bedtime. However, there is relatively little data to support the efficacy of taking melatonin supplements for sleep in other settings, partly because the source and dose of melatonin in supplements are not standardized or regulated. Ramelteon, a prescription melatonin agonist, is used for treating insomnia and may offer some benefit in the transient circadian rhythm disruption of jet lag.

Normal Sleep Regulation

Normal Sleep Regulation


Popular remedies for jet lag include:

Drinking coffee to stay awakeCaffeine has been shown to help reduce the effects of sleepiness associated with jet lag. However, it does not improve sleep, and in a slow-release formula, caffeine can actual generate less restful sleep. So a cup of coffee won’t cure jet lag, but it might help provide some alertness to counteract it. Similarly to caffeine, alcohol disrupts the sleep cycle by disrupting sleep architecture. Alcohol often makes people feel sleepy, but it impairs their rest. So both caffeine and alcohol can further upset the sleep schedule!

Getting plenty of sunshineLight exposure is the main connection humans have to the 24 hour day, so it makes sense that getting light (especially at the right time of day) would help resynchronize the biological clock. This clock can be moved about one hour closer to normal each day using light cues. For those who traveled east, and cannot fall asleep until much later in the night, it is important to get exposure to bright light in the morning. For those who traveled west and are sleepy too early in the evening, it is important to get bright light in the late afternoon, and dim light in the mornings.

and finally, refusing to change your schedule. For individuals traveling more than 5 time zones for a 2 day stay, studies have found that those who maintain their “home” sleep schedule and do not try to adjust fare better than those who try to adapt to local time! Of course, one of these studies also found that people prefer trying to adapt, for social and convenience reasons.

Whatever inspires you to next get jet-lagged, keeping in mind the physiologic basis will give you the best tools for recovering. Happy travels!

Cortical Basal Ganglionic Degeneration

This post is provided courtesy of K. T. Weber, Drexel University College of Medicine Class of 2013:

Cortical Basal Ganglionic Degeneration (CBGD) is a rare neurodegenerative disorder that affects both the cerebral cortex and basal ganglia, resulting in a rapidly progressive and devastating combination of movement disorder and dementia.

CBGD shares features with other, more common, neurologic illnesses: Like Parkinson’s disease, it often presents asymmetrically, with a tremor, rigidity or dystonia. Like Alzheimer’s disease, there are subtle early cognitive and behavioral changes. However, CBGD progresses more rapidly than these other conditions, ultimately involving the other limbs and causing more cognitive dysfunction. Furthermore the Parkinsonian features of CBGD tend not to respond to dopaminergic medications.

Patient with CBGD, showing rigidity, paucity of movement, and myoclonic jerks in the left arm

One of the distinctive features of CBGD is alien limb phenomenon. Alien limb is characterized by a “loss of agency” in the affected limb. The patient is able to feel sensation in the limb, and movement is preserved, but the patient no longer recognizes the limb as his or her own. This same aLien limb or (more commonly an alien hand) syndrome can also result from separation or dysregulation between the brain’s hemispheres, for example after surgical division of the corpus callosum for severe epilepsy.

Patient with CBGD, showing rigidity, dystonic posturing and Alien limb phenomenon (the patient said the left arm was “moving on it’s own”)

In popular media, Dr. Strangelove struggled with an alien limb that was no longer under his control.

However, the movement disorder is only half the story, and symptoms also include behavioral changes, cognitive decline, and abnormal speech. Behavioral changes may involve personality changes, mood problems, like depression and agitation, or the development of new compulsive behaviors. Language problems often begin with difficulty finding words (“anomia“) and may progress to an inability to speak.

The disorder is currently classified as a “tauopathy” in the same family of diseases as Pick’s disease, progressive supranuclear palsy (PSP), and even Alzheimer’s disease.

Although the diagnosis of CBGD is mostly clinical, there are some diagnostic tests that may helpful, such as asymmetric cortical atrophy on brain imaging or asymmetric slowing on EEG.


MRI showing right hemispheric atrophy

EEG showing L hemispheric slowing

EEG showing R hemispheric slowing

However, a definitive diagnosis can only be made by examining brain tissue at autopsy.

Pathology of CBGD (A) In the neocortex, ballooned neurons with displaced nuclei and pale cytoplasm (arrow) are common. (B) Immunostaining detects diffuse accumulations of tau protein in a peripheral distribution in a ballooned neuron. (C) Neuron loss and gliosis are often severe in deep nuclei, including the substantia nigra. (D) Diffuse cytoplasmic accumulation of tau protein is seen in neurons of various sizes in the neocortex (arrow, panel D), nucleus basalis (E) and striatum (F), as well as other locations. (Panels A,C from sections stained with H and E, remaining panels from sections immunostained with primary antibodies to tau).

Pathology of CBGD (A) In the neocortex, ballooned neurons with displaced nuclei and pale cytoplasm (arrow) are common. (B) Immunostaining detects diffuse accumulations of tau protein in a peripheral distribution in a ballooned neuron. (C) Neuron loss and gliosis are often severe in deep nuclei, including the substantia nigra. (D) Diffuse cytoplasmic accumulation of tau protein is seen in neurons of various sizes in the neocortex (arrow, panel D), nucleus basalis (E) and striatum (F), as well as other locations. (Panels A,C from sections stained with H and E, remaining panels from sections immunostained with primary antibodies to tau).

There are no effective treatments for CBGD, and therapy is aimed at symptomatic relief. The movement disorder, unlike Parkinson’s disease, does NOT respond well to levadopa, so other medications are used to help control the tremors and stiffness in the limbs. Beta blockers (propanolol), benzodiazepines (clonazepam), and gabapentin may have some efficacy in controlling tremor. Baclofen (a GABA agonist) is used to treat spasticity of many different causes and may provide some relief to patients with CBGD. Additionally, the depression, anxiety and agitation due to degeneration the cortical areas of the brain are critical therapeutic targets, and often respond to the first line therapies, including SSRIs and other antidepressants.

In summary, CBGD is a rare, progressive neurodegenerative disease. Recognizing the constellation of symptoms of CBGD from its more common cousins helps patients by identifying all elements of the disease progression, and can improve quality of life by addressing each of the related symptoms.

Charles Bonnet Syndrome, when the blind start to see things

Face of a man in a distorting mirror
The Charles Bonnet Syndrome, is an uncommon syndrome characterized by visual hallucinations that causes blind people to see things.

Charles Bonnet Syndrome affects 10-50% of patients with significant visual loss, who suddenly develop vivid, complex recurrent visual hallucinations, often “lilliputian” hallucinations (where characters or objects are smaller than normal), of faces, people, artoons, animals, or even trees and inanimate objects.

The syndrome is named after Swiss naturalist Charles Bonnet, who in 1769 described this phenomenon in his 89-year-old grandfather, nearly blind from cataracts in both eyes, but claiming to see men, women, birds, carriages, buildings, tapestries, physically impossible circumstances and scaffolding patterns

It is felt by some to be a visual release phenomenon – images generated by regions of the brain deprived of normal sensory input.

There is no known effective treatment, but symptoms usually resolves within a year or 18 months, and most patients are simply reassured to hear it is a normal phenomenon.

Watch a televised lecture by Dr Oliver Sacks entitled “What hallucination reveals about our minds”:

Click here for a link to a review of Dr Sacks’ book “Hallucinations”.

Click here to link an NPR story on Charles Bonnet syndrome entitled “Blind Man ‘Sees'”.

Dystextia, A new neurologic symptom for the new year


Neurology is laden with complicated terminology and eponyms.  For example, the terms aphasia or dysphasia indicate difficulty with verbal communication, most often from acute stroke affecting the dominant hemisphere.  The term apraxia indicates a disorder of motor planning causing an inability to perform a certain specific motor tasks even though strength is otherwise normal.  Dystextia is a term that has recently been coined to indicate the inability to create a coherent text message.

In a recent publication, Harvard physicians Ravi Rao and Klein describe an evolving stroke in a young woman manifest by dystextia:  A healthy 25-year old right-handed pregnant woman at 11 weeks’ gestational age, was brought to the emergency department after sending her husband a series of confusing text messages regarding their baby’s due date:

H: So what’s the deal?
P: every where thinging days nighing
P: Some is where!
H: What the hell does that mean?
H: You’re not making any sense.
H: July 24, right?
P: J 30
H: July 30?
P: Yes
H: Oh ok. I’m worried about your confusing answers
P: But i think
H: Think what?
P: What i think with be fine

Her brain magnetic resonance imaging showed an acute stroke in the left insular cortex:
Untitled-1 copy

Similar but transient problems texting caused by both aphasia and apraxia were previously reported as dystextia caused by complicated migraine by New Zealanders Whitfield and Jayathissa in their 2011 paper.

However, it was a 2006 paper published in the Irish medical journal by Catwood, King and Sreenam that first used the term dystextia, resulting from simple loss of left hand dexterity in a 40-year-old man with a right hemispheric stroke, which then slowly recovered over time:

In sum, young adults are spending more time texting and tweeting than talking or performing other daily activities.  We now have a descriptive term for when they have a neurologic event or process that prevents them from doing this.  However, it’s important to recognize that dystextia is a symptom, not a diagnosis, and can be caused by a variety of neurologic problems including aphasia, apraxia or simple loss of dexterity.