Limbic Encephalitis

Post prepared by Precious Ramirez-Arao, Monmouth Medical Center PGY3

A 60 year-old female was found lethargic lying in a pool of feces by roommate.

EMS was called and was immediately brought to the hospital.

In the emergency department she had a witnessed generalized tonic-clonic seizure.

Her roommate relates she had episodes of confusion and short-term memory loss over the past few weeks.

She remained lethargic over the next 72 hours in the hospital.

48-hour EEG monitoring showed diffuse 2 to 3 Hz delta slowing with periodic lateralized epileptiform discharges emanating from the left frontal temporal region.

PLEDS

T2 weighted image of the brain showed signal abnormality of the left mesial temporal lobe and the pulvinar with diffusion restriction in the left hippocampus consistent with limbic encephalitis.

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Limbic encephalitis (LE) is a subacute syndrome of seizures, personality change and cognitive dysfunction, typically evolving over days to weeks.

Autoimmune and paraneoplastic forms have been described. The most common neoplasms associated with paraneoplastic LE are lung cancer (usually small cell), thymoma, ovarian or testicular teratoma, breast cancer and Hodgkin lymphoma. The associated autoantibody depends on the tumor type. Lung cancer and thymomas are associated with anti-VGKC while ovarian or testicular teratomas are associated with antiNMDA antibodies.

Neurologic symptoms can precede oncologic diagnosis for several months to years and initial CT scans are typically unrevealing.

Nevertheless, prompt and thorough evaluation for malignancy including PET and CT scan of the chest, abdomen and pelvis should be initiated. Symptomatic treatment includes corticosteroids, plasmapharesis and intravenous immune globulin.

 

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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

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Introduction

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:

serotonin1

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.

Mechanism

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

Diagnosis can be made using the Hunter Serotonin Toxicity Criteria:

serotonin2

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.

Treatment

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.

Prognosis

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.

Prevention

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

Warning

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.

Prosopagnosia

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Memo to Hollywood: Don’t take it personally if Brad Pitt has no memory of meeting you. The World War Z actor, 49, apparently has a difficult time recognizing people’s faces. In fact, he thinks he may suffer from prosopagnosia, or face blindness.

Speaking about the problem in his much-talked-about interview for Esquire magazine’s June/July issue, Pitt says that even if he’s had a “real conversation” with someone, he’ll forget what the person looks like almost as soon as he or she walks away. “So many people hate me because they think I’m disrespecting them,” the actor confesses to the mag.

Prosopagnosia is a rare brain disorder that impairs the ability to recognize faces without affecting other aspects of visual processing.  It is usually caused by a lesion affecting the fusiform gyrus such as stroke or head trauma, although there are even rarer congenital cases.

Perhaps the best known case is “Dr. P.” in Oliver Sacks‘ 1985 book The Man Who Mistook His Wife for a Hat:

Dr P. was a musician of distinction, well-known for many years as a singer, and then, at the local School of Music, as a teacher. It was here, in relation to his students, that certain strange problems were first observed. Sometimes a student would present himself, and Dr P. would not recognize him; or, specifically, would not recognize his face. The moment the student spoke, he would be recognized by his voice …….. At first these odd mistakes were laughed off as jokes, not least by Dr P. himself …….. His musical powers were as dazzling as ever; he did not feel ill—he had never felt better ……. The notion of there being ‘something the matter’ did not emerge until some three years later, when diabetes developed. Well aware that diabetes could affect his eyes, Dr P. consulted an ophthalmologist, who took a careful history and examined his eyes closely. ‘There’s nothing the matter with your eyes,’ the doctor concluded. ‘But there is trouble with the visual parts of your brain ……… ‘What seems to be the matter?’ I asked him at length. ‘Nothing that I know of,’ he replied with a smile, ‘but people seem to think there’s something wrong with my eyes.’ ‘But you don’t recognize any visual problems?’ ‘No, not directly, but I occasionally make mistakes.’

Dr P. illustrates another important symptom in cognitive neurology, anosagnosia. Dr P. is himself completely unaware that he has a problem, he compensates without even knowing it.  It is his wife and students that encouraged him to seek medical attention.

Another reason to take snoring seriously! Sleep apnea linked to strokes.

sleepdisorder

Sleep apnea, the disorder that causes a person to stop breathing suddenly while sleeping, is already known to increase the risk of high blood pressure, heart failure, and daytime sleepiness.

seep apnea consequences

A new study suggests that the sleep disorder is also linked with small brain lesions and a symptomless form of stroke, known as silent stroke.

In the study, 56 men and women ( aged 44 to 75 years) who’d had a recent stroke or TIA underwent overnight polysomnograms.  91% had sleep apnea.

Furthermore, having more than five episodes of sleep apnea in a night was linked with having multiple extra “silent strokes” on their brain imaging studies.

silent stroke

Silent strokes don’t cause any symptoms as they occur, so a person typically doesn’t know he or she has suffered one, but they can eventually lead to memory loss and difficulties with walking, as their effects accumulate over the years.”

Yet another reason to take the on-line sleepiness test, and if your score is >10 see a sleep specialist and/or get an overnight polysomnogram in a certified sleep laboratory.

Memory Loss? Better check that medication list!

Memory Loss

Alzheimer’s disease is the commonest cause of memory loss and dementia.   We do not yet fully understand what causes Alzheimer’s.  However, we do know that the neurotransmitter acetylcholine is important in brain processing and memory.  We also know that the acetylcholinesterase inhibitors (drugs like Aricept<donezepil> , Exelon <rivastigmine> and Razadyne <galantamine>), which inhibit the breakdown of acetylcholine, do provide a symptomatic improvement in affected patients.

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acetylcholine

 

It is also known that many drugs can cause and/or exacerbate memory loss in elderly patients:

Anticholinergics block the effects of acetylcholine, causing confusion. They also negate the beneficial effects of aceylcholinesterase inhibitors in Alzheimer’s patients.  These drugs are commonly prescribed for urinary frequency and urgency, and include Ditropan <oxybutynin> and Vesicare <solifenacin>.  The tricyclics, including Elavil <amitriptyline> and Pamelor <nortriptyline>, commonly prescribed for insomnia and headaches, also have anticholinergic properties.

Benzodiazepine drugs like Xanax <alprazolam> Restoril <temazepam> and Klonopin <clonazepam>, most commonly prescribed for anxiety and insomnia, can also cause and/or exacerbate memory loss because of drowsiness and inattention.

A recent study of Alzheimer’s patients living independently in the community showed that as many 17% were taking anticholinergic drug and almost 9% were taking benzodiazepines.

As if that wasn’t bad enough, 16% of patients were taking both an acetycholineresterase (cholinergic) and an anticholinergic drug at the same time!

The bottom line here is that you should always bring a complete and updated list of all your medications with you to doctors appointments!

med list

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Click here for a link to the full article.