Magnetic Brain Stimulation Might Help Stroke Rehab?

Repetitive transcranial magnetic stimulation (rTMS) of the brain has been used to treat a variety of neurologic and psychiatric disorders including depression and dytonia.

A new study published this week suggests that it might also help speed recovery of speech and language in stroke survivors.  The  study included 24 stroke survivors with aphasia. Thirteen of them received transcranial magnetic stimulation (TMS) for 20 minutes every day for 10 days followed by speech therapy.  The remaining 11 received a “sham” brain stimulation.

Patients in the TMS group showed three times greater improvement than those in the sham stimulation group.

Find out more here.

New Hope for Nerve Injury Patients

Nerves are complicated structures, made of many axons (the actual connections or wires) some surrounded by a layer of myelin shealth (insulation), all bundled together with connective tissue into a giant cable.

Nerve injuries come in different varieties, depending on the mechanism and severity of the trauma:

The three categories of nerve injury Neurapraxia (top), Axonotomesis (middle) and Neurotmesis (bottom).

The mildest injury is neurapraxia, which is a short area of segmental demyelination.  Because the underlying axon is left intact, recovery can occur within days to week by simple remyelination.

The more severe injuries axonotomesis and neurotmesis involve axonal injury.  Once the axon is injured, the whole segment distal to the injury undergoes a pre-programmed process of degeneration called Wallerian degeneration:

Wallerian degeneration – the axon distal to (right of) the injury degenerates.

Even if the nerve injury is repaired, or gets better on it’s own, the axon has to grow back all the way from the injury site to the end of the nerve at the muscle before functional recovery can occur.

Even if a severed nerve is repaired (in this case by direct suturing), the axons have to regrow down the entire distal nerve segment before functional recovery can occur

Axonal regrowth is slow, occurring at a rate of no more than 1mm/d.

If we have a patient with a proximal nerve injury, for example a brachial plexus injury:

nevre injuryAxonal regrowth will have to occur over 600-800mm to restore function to the hand, and that will take more than 2 years, by which time the muscle may have deteriorated so much it can no longer receive a new nerve supply and recover.

However, new research in animals has led to a technique that reconnects the severed ends of a nerve, allowing it to begin carrying messages again very quickly, restoring conductivity before Wallerian degeneration has a chance to begin. This allows for almost immediate function recovery after nerve repair surgery.

In the experiments, the severed nerve are exposed and treated with chemical compounds to keep the axonal ends open, then the two nerve ends are sutured together, and are finally treated with more chemicals that cause the nerve ends to fuse.  Rats treated with his technique got better as soon as they began to recover from the surgery.

Researchers hopes to try the approach on people within a year.

Click here for a link to the full story.

Shouldn’t I have a brain MRI, doctor?


Migraine is extremely common, with a lifetime incidence of 43% in women and 18% in men, and a median age of onset of 24-5.

The vast majority of headache patients have migraine and need a careful history & physical examination, followed by appropriate treatment, not a brain imaging study.

Studies have shown that a brain imaging study will disclose an “abnormality” in about 1% of unselected headache patients, similar (if not less) than asymptomatic test subjects.

Furthermore, there are potential complications involved with brain imaging:  Some patients are claustrophobic and require sedation, even a general anesthetic.  Many “abnormalities” are innocuous, unrelated to the headache and do not require treatment.  However, these headache patients with such  “incidentalomas”  are left with the conclusion that there is something wrong with them, and may be subjected to further unnecessary follow-up studies.  A few end  up getting unnecessary invasive tests, which actually hurt them.

However, not a day goes past without a migraine patient asking me for a brain imaging study, or for that matter a patient referred to the office worried about an “incidentaloma” identified on a brain imaging study which should never have been done in the first place.

That’s not to say brain imaging is always unnecessary in every headache patient.


Carefully selected patients with the following “red flag” characteristics might still need a scan:


This approach is supported by the American Academy of Neurology, whose position is that neuroimaging usually is not warranted for patients with migraine and normal neurologic examination, only for patients with atypical headache features.

Find out more about migraine and headache here.

Dr Holland and Monmouth Neuroscience Institute’s TIA Rapid Evaluation Center Honored at the 2013 Heart Ball

The American Heart Association and American Stroke Association gathered to recognize Dr. Neil Holland and Dr. June Duck as this year’s medical honorees at the annual Heart Ball on June 21 at the Ocean Place Resort and Spa in Long Branch.


Drs Holland and Duck with their awards.

Dr. Holland was recognized for excellence in stroke care. Commended for his role in developing a TIA and Minor Stroke Rapid Evaluation Center, Dr. Holland has focused care to optimize stroke prevention without the need for hospitalization in high-risk patients.



The Monmouth TIA Center Team – L to R – Neuroscience ARNP Florence Armour, Hospital VP Shirley Hwang, Program Director Dr Holland, Neuroscience Coordinator Felesia Swanson & Dept of Medicine Chairman Dr Allan Tunkel


Dr Holland with his partners – L to R – Drs Gennaro, Anayiotos, Gilson, Holland, Herman, Davis, Mendelson & Ponce.
The success of the TIA Center is the result of close cooperation between hospital administration, all of the doctors in the practice, the Emergency Room, and many many other members of the hospitals medical and technical staff.

Find out about Monmouth’s Stroke Service and TIA Center.

Blackout – was it a fit or a faint?

People generally experience a blackout (temporary loss of consciousness) from one of two common problems: (1) Insufficient blood flow to the brain (syncope)  or (2) Abnormal electrical activity within the brain (seizure).


Syncope (or a faint) is caused by insufficient blood flow to the brain because of low blood pressure.  There may be a prodrome of dizziness loss of vision and hearing weakness, flushing, nausea (sometimes referred to pre-syncope).  Then there will be overt loss of consciousness that leads to the faint.  The affected patient will typically fall by dropping forwards from loss of muscle tone. The affected patient might look pale and clammy, and will usually come around quickly of they are allowed to lay down on floor allowing blood flow to return to the brain.  Syncope can be caused by dehydration, irregular heart beat, or emotion (vasovagal or “neurocardiogenic” syncope).


A seizure (or a “fit”) is caused by abnormal electrical activity in the brain, usually accompanied by a clinical event that can vary from a brief loss of awareness (an absence seizure or “petit mal”) to loss of awareness with thrashing limb movements (a tonic-clonic or grand mal seizure).  A generalized tonic-clonic seizure will usually be associated with increased muscle tone, so the patient will stiffen up and fall backwards not forward and may bite their tongue.  The eyes will be open, and their may be loss of bladder and bowel control.  There may be flailing limb movements that lead to injury.  After the seizure stops, the patient will usually be confused or dazed, and not come around immediately like the syncope patient.


Here is a table that emphasizes the differences between fits (seizures) and faints (syncope):



If you have experienced a blackout, what should you do? A simple faint in an otherwise young healthy person may not need emergent medical care.  However, syncope in an older person with a cardiac history, or syncope associated with chest pain and breathlessness could indicate a heart problem and usually justify an emergency room visit.  Similarly a new onset seizure in somebody not previously know to have epilepsy should justify an emergency room visit.

Lifestyle changes that reduce migraines


Migraines affect about 1 billion people around the world.  About 18% of women and 6% of men experience at least one migraine every year, with a lifetime risk of 43% and 18% respectively.

Triggers that can bring on a migraine attack include: Alcohol, Certain foods, Dehydration, Fasting, Lack of sleep, Too much sleep, Irregular sleeping patterns, Stress, Menstruation, Smells (perfumes), and Weather changes.

Other than taking abortive medications, which can sometimes hurt more than they help, here are some things you can do to prevent headaches:



Tai Chi Group

Many migraine patients avoid doing exercise because physical exertion may be one of their triggers. However, yoga, tai chi and other mind/body exercises can be useful in managing migraine.


Food and drink


Certain foods and drinks can trigger migraine attacks -you need to find which foods or drinks trigger your attacks and either avoid them or consume them less.  Common foods/drinks linked to migraines are: Red wine, Caffeine, Chocolate, Mature cheese (containing high levels of tyramine), Food additives & preservatives (such as aspartame and monosodium glutamate)




People who have a lot of stress in their lives are more likely to sufferer from frequent headaches, and migraine sufferers should find ways to lower that stress.



Man sleeping

Getting enough sleep is vital for good migraine control. Sleep deprivation has been shown to be closely linked to the frequency and severity of migraine attacks in some patients.  People who sleep less than six hours a day are more susceptible to headaches. However, too much sleep can also make things worse.  Migraine sufferers should try to go to sleep and wake up at the same time every day, even on weekends.

Restless Leg Syndrome and early death?


A recent study in Neurology got a lot of press recently when it suggested that men with restless leg syndrome (RLS) are at a 40% higher risk of death from all causes than similar men  without the condition.  Dr. Xiang Gao, and his colleagues at Harvard, followed 18,000 men over 8 years and found evidence of increased mortality in men with RLS, even when controlling for other risk factors.

RLS typically causes discomfort in the legs and feet during the night.  This discomfort is often relieved by moving the legs, rubbing the feet, or walking around.  It often can impact sufferers’ ability to fall asleep and stay asleep.  In severe cases, it can affect the arms and can also occur during the day.

There has not been any convincing evidence that it is otherwise dangerous, however.  In fact, several previous studies looking at the condition did not show a link to early death.

Because RLS is shown to cause sleep fragmentation and insomnia, it could be argued that the increased mortality risk seen in this study is a result of generally poor sleep, and not RLS per se.  Therefore, these results should be interpreted with extreme caution.

This study, if nothing else, indicates the need for further research on this elusive disorder.

Why it happens and what it means are still generally unknown.

It can profoundly impact sleep quality and therefore quality of life.

There are some who do not believe RLS is a legitimate disorder. Those who live with the disorder would disagree.

RLS can be quite debilitating.  However, many treatment options exist for RLS and many of the symptoms can be improved.

If you think you may have RLS, seeing a neurologist or a sleep specialist is often the best step.

Epilepsy surgery and functional MRI



Epilepsy surgery is an option for patients with intractable partial onset seizures that are not controlled by oral medications.  Epilepsy monitoring is used to localize the seizure focus, often a lesion or abnormal area of brain located in the temporal lobe.  That part of the brain is then carefully removed to prevent future seizures:

seizure surgery2

A patient with a brain abnormality in the R temporal lobe (top) undergoes brain surgery to remove that area of brain and prevent future seizures.

Epilepsy surgery is very effective and yet still underutilized for treating seizures.

Left temporal lobe resections are more risky that right-sided cases, because the left hemisphere controls language functions in most (even left handed) patients.  Surgeons have to be very careful planning seizure surgery on the left side to be sure that they do not damage brain critical for speech and language and leave the patient with aphasia.

That’s where functional magnetic resonance imaging (fMRI) comes in.  fMRI goes beyond the conventional imaging of brain structure, and can actually localize regional brain functions by detecting changes in regional blood flow in response actual or imagined activity.

fMRI is increasingly being used to evaluate candidates for epilepsy surgery by identifying important functional regions within the brain, including unpredictable patterns of functional reorganization, to prevent unexpected post-operative deficits.  Click here for a link to a paper with illustrative cases.

Rituximab for Secondary Progressive MS?


Multiple sclerosis comes in different varieties:



Many patients with MS have discrete relapses, which then resolve either partially or completely resolve, and are separated by periods of disease inactivity.  We call this relapsing-remitting (a) or progressive-relapsing (b) disease.

Most of the “disease modifying” drugs currently used in MS work by preventing discrete relapses (and by preventing relapses) they will prevent the progressive acquisition of disability which can accompany each relapse in these types of MS.


However, there are other MS patients develop progressive disability without discrete relapses.  This can occur after a relapsing remitting phase, so-called secondary progressive MS (c).  Or patients can start right out with progressive disease without any history of discrete relapses, so-called primary progressive MS (d).

Most disease modifying drugs are of little benefit for progressive disease, and treatment has been predominantly symptomatic, with dalfampridine and symptomatic treatments for spasticity.

The chemotherapy drug mitoxantrone was found to have some efficacy for treating secondary progressive MS, but the duration of therapy is limited to 2 years because of toxicity.

New data presented at the fifth Cooperative Meeting of the Consortium of Multiple Sclerosis Centers and the Americas Committee for Treatment and Research in Multiple Sclerosis this week suggests that the chemotherapeutic agent rituximab may also stabilize or even reverse disability in secondary progressive MS.


What causes vertigo and nystagmus?


Dizziness is a vague term than different people use to indicate a variety of experiences including lightheadedness, unsteady gait and vertigo.

Vertigo is a more precise term, which indicates a sense of false movement – if feels like the world is moving (using spinning).

To understand what causes vertigo, you first have to understand the vestibular system, and the vestibular ocular reflex (VOR).

The vestibular system is made up of 2 systems of semicircular canals, within the inner ears (or labyrinths), designed to detect head position and movement:

inner ear


Each semicircular canal works like a spirit level to determine head position in it’s plane:

spirit level


The VOR is a connection between the vestibular system and the muscles that move the eyes, which allows us to seamlessly compensate for every little head movement.


Life without a normally functioning VOR would be something like this:

For the sake of simplicity, we’re just going to talk about the horizontal canals.

There is tonic input to the brain from each side at rest.

When the head moves to the right, input from the right side increases, input from the left side decreases, this creates a mismatch between the two sides, and brain knows the head is moving:

The VOR then provides a reflex corrective eye movement to the left, so that the eyes keep looking in the same direction to maintain fixation:

normal VOR


Now, let’s say there’s a medical problem like a viral infection or a tiny stroke, that injures the L sided labyrinth, we call this labyrinthitis or acute labyrinthine failure.  This reduces tonic input from the damaged L side, and will lead to the same mismatch as if the head were turning to the right side:


This, in turn, will:

1. Fool the brain into thinking the head is turning to the right side, creating an illusion of movement, “vertigo” .

2. Lead to unnecessary “corrective” eye movements to the L side, which (in the alert patient) will be followed by a voluntary eye movement back to the R to maintain fixation.  This combination of a slow drift of the eyes to the underactive side, and a rapid eye movement back to the middle is know as nystagmus.


Nystagmus from L labyrinthine failure – slow eye drift to L, then rapid eye movement back to R side.

We can reproduce this phenomenon with the cold caloric – the cold water causes temporary vestibular hypofunction, vertigo and nystagmus:


Ultimately, the brain will “reset” and the vertigo and nystagmus improve.  During this phase, stable visual input (which says the world is stationary) overcomes the abnormal vestibular input (which says the world is moving).  You are probably aware of this phenomenon from sea and car sickness –  You are less likely to get sick if you are on deck (looking at the horizon) or in the front seat of a car (looking out the window).