The Neurology of JFK’s Assassination

As a devout conspiracy theorist, I could not resist posting about the John F. Kennedy assassination during its 50th anniversary.


This story contains at least 3 neurological issues of interest.


First, there’s the head wound, and what it tells us about the location of the shooter:

Conspiracy theorists have stressed witness testimony that the back of Kennedy’s head was blown out, suggesting a shot from the Grassy Knoll.

Lone assassin theorists have stressed the photographic evidence and the autopsy x-rays, which show the back of the head intact. The panel (inserted above) shows four of the dozens of versions of Kennedy’s head wound.

Click here to find out more.


The Manchurian Candidate 1

Second, even if you believe Lee Harvey Oswald was the lone assassin, some conspiracy theorists would have you believe he was a Manchurian Candidate, manipulated by mind-control experts to carry out the assassination of JFK.

These theories are supported by what is known about the CIA’s experiments with mind control in the 1950s, and Oswald’s alleged CIA connections.

Click here to read more about this.



Finally, there is Jack Ruby‘s murder of Lee Harvey Oswald:

The matter of neurologic interest here is that Ruby’s defense at trial was based on an abnormal electroencephalograph.

Defense expert Frederick Gibbs, one of the pioneers in the use of electroencephalography for the diagnosis and management of epilepsy,  testified that Ruby’s EEG showed right temporal 6/s sharp waves, and that this was evidence of “psychomotor epilepsy”.


Gibbs suggested that affected patients manifest personality instability, lack of emotional control, convulsive and excessive types of behavior.  He, and other physician experts at the trial further postulated that Ruby killed Oswald during a fugue state induced by a psychomotor seizure.

Middle finger

This image of Ruby shooting Oswald was used at trial – Ruby is seen using his middle finger to pull the trigger, with his left hand thrown out in the opposite direction, supposedly indicating a seizure.

The prosecution’s neurology expert disagreed, stating that the EEG findings were a “slight abnormality” and didn’t indicate epilepsy.  Furthermore, he indicated that Ruby’s demeanor and behavior, as described by witnesses, were not consistent with a psychomotor seizure.

Ruby was convicted, and sentenced to death.

Click here to find out more about the neurology at the trial.

This EEG “finding” is now known to be a normal variant with no clinical significance.

This case underscores the importance of treating the patient, not the test result, an adage well known to true clinicians everywhere.


Seizures from Art Exhibit, Latest Example of Photosensitive Epilepsy


Outside Gallery ZEE in Pittsburgh

A Pittsburgh art exhibit that closed this week after three people were treated for reported seizures.

Shaunda Miles, spokeswoman for the Pittsburgh Cultural Trust, said the exhibit titled “Zee” by Austrian artist Kurt Hentschlager is closed indefinitely.


The installation, part of the Cultural Trust’s Pittsburgh International Festival of Firsts, was scheduled to run through Oct. 27.

It includes heavy fog and intense strobe effects, and attendees must sign a waiver before entering.

Click here to find out more about this story.

Photosensitive Epilepsy

Epileptic seizure types can be  induced in certain susceptible patents by photic (or visual) stimuli,  usually flashing lights or rapidly changing/alternating images . Some famous examples have included:


An animated segment of a film promoting the 2012 London Olympics:

Flickering fluorescent lighting:

Video Games:

Strobe lights in clubs:

Photosensitive seizure only occur in a small proportion of patients with generalized epilepsy, and those patients will usually know they are susceptible based on their routine diagnostic EEG, which will usually include intermittent photic stimulation as part of routine testing.
Click here to find out more about seizures and epilepsy

Do you take an antidepressant medicine? – If the answer is yes, you should know about serotonin syndrome

Post written by Dr. Hadi Razjouyan, PGY III Internal Medicine Resident at Monmouth Medical Center



Serotonin syndrome is a rare and potentially life-threatening toxic state caused by excessive serotonergic activity in the nervous system.
It was first described in 1960s in studies of antidepressant medications and classically consists of a triad of mental status changes, abnormalities of muscle tone, and autonomic hyperactivity. However, clinical manifestations can be diverse and nonspecific, leading to misdiagnosis. Most reported cases are in patients using multiple serotonergic drugs, or who have had considerable exposure to a single serotonin-augmenting drug:


Medications that may contribute to serotonin syndrome. (Ables AZ, Nagubilli R. Prevention, recognition, and management of serotonin syndrome. Am Fam Physician. 2010 May 1; 81(9):1139-42).

Epidemiologic features

It can happen in all age groups.
Its incidence is rising as the number and use of available serotonergic drugs are increased in clinical practice.


Potential mechanisms include increased serotonin synthesis or release; reduced serotonin uptake or metabolism; and direct serotonin receptor activation. Addition of drugs that inhibit the cytochromes (e.g. CYP 2D6 and/or 3A4) to therapeutic regimens of selective serotonin reuptake inhibitors (SSRIs) could be another mechanism.
The majority of cases are iatrogenic from synergistic medication use, although cases of self-poisoning with serotonergic agents also occur.


Diagnosis can be made using the Hunter Serotonin Toxicity Criteria:


Hunter’s rules for diagnosis of serotonin syndrome. (Ables AZ, Nagubilli R. Prevention, recognition, and management of serotonin syndrome. Am Fam Physician. 2010 May 1; 81(9):1139-42).

Symptoms can include anxiety, restlessness, confusion, sweating, muscle spasm or rigidity, rapid back and forth eye movement, shaking, fever, rapid heart rate, vomiting and diarrhea.

Symptoms can develop rapidly, within minutes of taking the drug, however, most patients present within couple of hours after a medication change or overdose.

Differential Diagnosis

The primary differential diagnosis of serotonin syndrome includes malignant hyperthermia, neuroleptic malignant syndrome, and anticholinergic syndrome. A complete history of the drugs or substances is helpful in ruling out these conditions. It is necessary to rule out initiation or change of dosage of dopaminergic drugs and other possibilities, such as infection, metabolic disorder, substance intoxication, or withdrawal. Other potential diagnoses include heat stroke, overdose of sympathomimetic drugs, delirium tremens, meningitis, encephalitis, thyroid storm, sepsis, or tetanus.


First, Recognize the disease
Next, Stop the offending agent(s)
In the meantime, Supportive care (treat hyperthermia, autonomic dysfunction)
Benzodiazepines may be used to treat agitation and tremor.
Sometimes may administer serotonin antagonists, cyproheptadine or chlorpromazine.
Patients with moderate or severe cases of serotonin syndrome require hospitalization.
Critically ill patients may require neuromuscular paralysis, sedation, and intubation.


If serotonin syndrome is recognized and complications are managed appropriately, the prognosis is favorable. The severity of the disease can range from mild to life-threatening situation. However, most cases are mild and do not require hospitalization and generally resolve within 1 to 3 days by withdrawal of the offending agent and supportive care. Patients with moderate and severe cases may require hospitalization.


Awareness of physicians and patients of the potential for toxicity from serotonergic drugs.
Always tell any doctor who prescribes you about all medications, herbal products and street drug you take.
When starting new medicine, have the pharmacist check for drug interaction
Avoiding the combined use of serotonin-augmenting drugs.
If you are already on medicine, do not take a new herbal or over-the-counter medicine without first checking with your doctor


If you have any symptoms of serotonin syndrome, please call your primary care physician and inform him/her of your suspicion before taking any steps.

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.

Monmouth Epilepsy Program Receives NAEC Certification

Monmouth Medical Center’s Epilepsy Program was awarded prestigious level 3 certification today by the National Association of Epilepsy Centers!

Monmouth certificateThe National Association of Epilepsy Centers (NAEC) is a non-profit  association with the primary objective of connecting people with epilepsy to specialized epilepsy care and epilepsy centers.

Founded in 1987 by physician leaders committed to setting a national agenda for quality epilepsy care, the NAEC educates public and private policymakers and regulators about appropriate patient care standards, reimbursement and medical services policies.

NAEC works in conjunction with existing scientific and charitable epilepsy organizations.

A third-level center must provide all the medical, neuropsychological, and psychosocial services needed to treat patients with refractory epilepsy to achieve certification.

Click here to find out more about Monmouth’s Epilepsy Program.

Click here to find out more about seizures and epilepsy.

Epilepsy and Seizures, What’s the difference?


What is a Seizure?

A seizure (or “fit”) is physical finding or change in behavior that occurs because of abnormal electrical activity in the brain.

When people think of a seizure, they usually imagine a generalized (or “Grand Mal”) tonic clonic seizure:

It is estimated that as many as 5% of all Americans will experience an epileptic seizure during their lifetime.


What is epilepsy?

Epilepsy results from a permanent change in brain tissue causing it to be too excitable, leading to repeated unpredictable seizures over time.

This can occur from a brain injury, such as head trauma, birth asphyxia or a stroke, brain tumor or can be genetic (something you were born with).

The prevalence of epilepsy is estimated to be 1-2% in the USA.


Not all seizures lead to epilepsy.

Why is the prevalence of epilepsy so much lower than the incidence of seizures?

The answer is that not all seizures will lead to epilepsy.

A seizure can be provoked by some extraneous factor such as high fever, medication, drugs and alcohol, or blood electrolyte disorder, which if addressed properly will not lead to further seizures.

However, a single seizure can also be the beginning of epilepsy, necessitating an anti-epileptic medication (or anticonvulsant) to prevent further episodes.


So, how do you tell if a first seizure is the beginnings of epilepsy?

All patients presenting with their first seizure should have a thorough evaluation, including a detailed history (from someone who observed the episode), physical examination, blood work, brain imaging study and electroencephalogram.

A seizure which begins with a focal onset, such as a warning (“aura”), unusual behavior (“automatism”), or focal movements just as turning the head to one side or jerking on one side of the body suggests the beginnings of epilepsy from an underlying brain injury or lesion.


Seizure with automatism (Partial Complex Seizure):

Note that the patient appears awake, but is not responding normally, and has lip smacking and pointing (the automatisms), indicating a focal (temporal lobe) seizure onset.  He seems confused and disoriented afterwards.


Seizure with focal motor activity:

Although the patient is unresponsive and jerking, note that the head is turned to the right and there are only right sided limb movements, indicating that the seizure is coming from the left side of the brain.


Some genetic seizure syndromes, like juvenile myoclonic epilepsy or absence epilepsy (“petit mal”) begin in childhood or adolescence, are associated with characteristic EEG findings, and indicate epilepsy which will be recurrent without treatment.

Absence seizure:

The child is talking, then suddenly stops and stares off into space, then suddenly resumes speech as if nothing happens. This is a typical absence seizure or “Petit Mal” from epilepsy and will recur without treatment.


There are physical signs which suggest an underlying neurocutaneous syndrome, and epilepsy:

Syndrome characterized by a facial port-wine stain, seizures, paralysis or weakness on one side, learning disabilities, and "calcifications" in the brain

Syndrome characterized by a facial port-wine stain, seizures, paralysis or weakness on one side, learning disabilities, and “calcification” in the brain

Genetically determined syndrome of epilepsy associated with     Areas of the skin that are white (due to decreased pigment) and have either an ash leaf or confetti appearance    Red patches on the face containing many blood vessels (adenoma sebaceum)    Raised patches of skin with an orange-peel texture (shagreen spots), often on the back

Genetically determined syndrome of epilepsy associated with: Red patches on the face containing many blood vessels (adenoma sebaceum) . Areas of the skin that are white (due to decreased pigment) and have either an ash leaf or confetti appearance . Raised patches of skin with an orange-peel texture (shagreen spots), often on the back . Small tumor like lesions at the nail folds (subunguual fibromas) .


Genetically determined epilepsy syndrome associated with fatty tumors, pigmented patches (including in the arm pits), and Lisch nodules in the iris.


The presence of an abnormal EEG in a patient presenting with a single seizure increases the chances of another seizure (epilepsy) and may warrant initiation of an anticonvulsant medication. This could be either a focal spike suggesting a partial onset seizure focus:
EEG spike
Or a burst of generalized spike wave activity, suggesting a genetic generalized epilepsy:


A patient with seizures and an abnormal brain imaging study is also more likely to suffer a recurrence and develop epilepsy:
Abnormal Brain MRIs in Epilepsy

However, if all the tests are normal, it can be hard to tell if a single unprovoked seizure is the beginning of epilepsy or not, only about 20-30% of these patients will have a recurrent event, so sometimes it is better to wait and see what is going to happen rather than rushing into starting an anticonvulsant medication here.


Where to get more help.

These are complicated issues and decisions which should only be made after consultation with a neurologist, preferably a neurologist with subspeciality training or certification in epilepsy at an epilepsy center.