Neurology

Researchers at Massachusetts General Hospital considered the neuroanatomy of peduncular hallucinosis, which usually involves very colorful and elaborate visions of people, animals and scenery.

Classically, the symptoms are caused by damage to the midbrain, pons or thalamus. The problem is that in actuality, lesions such as strokes don't usually just hit one little area, but involve more than one region.

The researchers looked at the magnetic resonance imaging of people with strokes that led to peduncular hallucinosis, and seeing what areas of damage these brains had in common.

The main site shared by 22 out of 23 cases was the central thalamus when studying all lesion overlap analysis, in areas called the intralaminar and paramedian nuclei. The right half of the brain was usually involved.

This initial study was followed by special functional MRI studies that showed a connection between this region and areas responsible for visual association in the back of the brain.

This finding ties together what has previously been a seemingly unrelated set of subcortical structures. Furthermore, the findings call into question the usual explanation for peduncular hallucinosis, that it is due to release of inhibition of the posterior visual cortices.

Instead, the researchers suggest that the hallucinations result from a pathological network transition from normal visual processing of the external world to internal visual imagery. Other suggested theories include a release of the dreaming stage of sleep into the waking state.

I confess that I had high hopes for trials of IVIG in the treatment of Alzheimer's. Preliminary evidence suggested that the medication could be very beneficial. Unfortunately, the results from the large clinical trial have shown no significant benefit between those who were taking the drug and those who were not. There were some significant findings in a group of patients who were positive for the gene ApoE4, but whether these results will be clinically meaningful remains to be seen.

Alzheimer's disease is a personally crushing illness that has the potential to overwhelm healthcare systems in the coming decade as populations age. Despite millions of dollars spent, the disease is stubbornly resistant to all treatments so far. In the face of numerous expensive defeats, many companies are reconsidering whether it is worth further attempts to cure Alzheimer's disease. For those already suffering from the disease, a cure cannot come quickly enough.

Postural instability is a cardinal symptom of Parkinson's disease, and stops many from even walking. Dancing, on the other hand, may be more helpful.

Ann McKee, a fourth year medical student at Emory University, presented results at the 2013 American Academy of Neurology's Annual conference that suggests that 30 hours of tango lessons helped Parkinson's patients with mobility and balance.

Even months after the training ended, benefits were still detectable. Only two participants fell during the 48 classes. All seemed to enjoy the classes as well.

Intriguingly, this isn't the first time dance has been suggested to help with Parkinson's disease. Earlier in March 2013, an Italian neurologist named Dr. Volpe described the benefits of Irish dancing in Parkinson's. He first noticed the effect in a gentleman with Parkinson's disease in 2010. Dr. Volpe suspected the benefit came from the different steps in the dance, which were different from the standard back and forth movement of walking.

Another possible explanation may be the rhythmic music, which could cue the brain to bypass the standard pathway involved with walking. Parkinson's disease involves abnormal rhythms in the basal ganglia, and perhaps the music can interrupt that signal.

Regardless of the reasons, people with Parkinson's disease may have something new to dance about.

A group has shown that an investigational drug called ecopipam relieved tics in adult patients after just eight weeks. The drug works on dopamine receptors, thereby addressing the neurological network theorized to underlie the symptoms of Tourette's syndrome.

According to Donald Gilbert, MD, MS, of Cincinnati Children's Medical Center, ecopipam reduced measures of tic severity by 20 percent.

Currently, drugs for Tourette syndrome are primarily antipsychotic medications such as haloperidol (Haldol), which can have severe side effects in some patients.

Many of the patients lost weight while taking ecopipram. Three patients had nausea, fatigue and sedation. Two others had insomnia and restlessness. Urges to perform a tic, mood, and obsessive-compulsive behavior was not changed.

These results remain preliminary, and require confirmation by a larger trial.

There are many reasons to feel dizzy, and anxiety is one of the most common. Panic attack involves sudden and recurrent episodes of at least four of the following symptoms:

1. Chills or hot flushes
2. Feeling separate from reality or your own person
3. Dizziness or lightheadedness
4. Fear of dying
5. Fear of losing control
6. Feeling of choking, chest pain or other discomfort
7. Nausea
8. Palpitations
9. Paresthesia
10. Sensations of shortness of breath
11. Sweating
12. Trembling or Shaking

Some physicians suspect that fewer than four symptoms may also be common, in which case the episodes are called limited-symptom attacks.

Over half of people with panic attacks feel dizzy during the episode. To further confuse the issue, many people who feel dizzy with panic attacks have also had another problem with their vestibular system in the past.

A common pattern is that someone will either have disturbing thoughts that make them feel dizzy, or feel dizzy and then worry to the point that they have disturbing thoughts. For example, when frightened many people breathe quickly, and breathing quickly can disturb the chemistry of the body in a way that makes people feel woozy. This woozy feeling can make some people panic even more. The result is a spiral where feelings of panic and dizziness feed on each other, making both symptoms increasingly severe.

The best treatment for this kind of dizziness is behavioral therapy and treatment for anxiety. Such therapy can relieve both the dizziness and the anxiety associated with that symptom.

For more on dizziness, try the following:

Is My Dizziness a Side Effect?

Dangerous Causes of Dizziness

Vestibular Migraine

I've written a bit already about epilepsy in children under the age of two. This month, I've written more on epilepsy in children older than two years. This kind of age division is artificial, and some syndromes actually overlap. Still, dividing by age like this does help to make sense of the bewildering number of seizures syndromes out there, of which I'm only discussing some of the most common or best known.

Another common way is to distinguish between "partial" seizures, which start in one part of the brain and do not immediately cause loss of consciousness, from "general" seizures which seem to begin everywhere at once, and in which consciousness is quickly lost.

Yet another division is between "symptomatic" epilepsy and "asymptomatic" epilepsy, terms sometimes used among doctors to distinguish those who have developmental problems caused by their epilepsy (symptomatic) from those who do not (asymptomatic). These terms are falling out of favor, though, since all seizures are symptoms, which can lead to confusion- for the most part, I will refer to symptomatic seizures as "serious" seizure syndromes, meaning that there is a high risk for developmental disability or early death. This is not to say that seizures alone are not serious, but in childhood epilepsy, "serious" and "benign" become more relative...

For more, read here:

Partial Epilepsy Syndromes of Childhood

Generalized Epilepsy Syndromes of Childhood

Serious Epilepsy Syndromes in Children

There are many neurological causes of hallucination, but few if any are well understood. Researchers at the 2013 American Academy of Neurology Annual Conference addressed the question of how the type and location of abnormal proteins in a dementia affected the risk of hallucinations. Formed visual hallucinations can accompany Parkinson's or Alzheimer's disease. Some studies suggest this is related to increased Lewy body pathology, which is classically associated with Parkinson's or Lewy Body Dementia. Sometimes, though, the misfolded proteins called Lewy bodies exist in brains of people with Alzheimer's as well, though Alzheimer's is usually associated with microscopic findings called amyloid plaques and neurofibrillary tangles.

The other argument is that the proteins are less important than the locations of those proteins. For example, limbic or temporal locations of the pathology may be more associated with hallucinations.

173 subjects with either Parkinson's disease or Alzheimer's disease were included in the study. 50 had formed visual hallucination, and 123 did not. Brains were later evaluated on autopsy. The researchers looked at the Lewy body levels, amyloid plaques, and neurofibrillary tangles. Overall, people with hallucinations died at a younger age, were more likely to be male, and were more likely to have Parkinson's disease with a higher medication dose than those without hallucinations. The more Lewy bodies that were present, the more likely someone was to have hallucinations. There was no difference in amyloid plaque burden between those who hallucinated and those who did not. Neurofibrillary tangles were actually more common in those who did not hallucinate.

In short, the areas most impacted by the brain seemed less important than the type of protein, but like other studies beforehand, there was a hint that damage to the temporal lobes were more involved with hallucinations.

Alleviating pain is one of the greatest missions of doctors everywhere. The mission is frustrating, though, because pain is very hard to measure.

At this time, a physician has to rely entirely on what the patient says about the severity of their pain in order to treat it. Unfortunately, as the television physician Dr. Gregory House was famous for saying, "People lie." House himself was an example of someone who was addicted to painkillers. Doctors are under enormous pressure to avoid contributing to the rampant opiate abuse epidemic in the United States, but at the same time want to help suffering patients.

It would be very helpful, then, to have a way to objectively measure pain so that doctors didn't have to just rely on what people told them. Unfortunately, past attempts have been limited at best. Many doctors now simply ask for the patient to give them a number on a scale of one to ten, which only modestly tries to disguise the complete subjectivity of pain.

A group headed by Dr. Tor Wager at the University of Colorado, Boulder, has now used functional MRI (fMRI) studies to recognize when someone was feeling pain. The study only studied pain experimentally induced by heat. Further studies will address whether this phenomenon is useful in patients.

The neuroimaging studies revealed involvement of structures such as the ventrolateral thalamus, the secondary somatosensory cortex, and the dorsal posterior insula. The work builds on previous studies that showed changes in similar areas. This study, however, demonstrated a pattern that was reliably specific and sensitive for individual people, not just large study groups. This means that the technique may have true and more immediate medical applications.

This technology goes beyond trying to confirm severe pain in those asking for potentially addictive medications. In fact, Dr. Wager expressed reservations about the imaging being used in such a fashion. Although physicians may wish for a "pain lie detector," this technology isn't quite rightf for that, and focusing on that use could take focus fro an even more important application. This could also be a way to check for pain in people who might not be able to say anything about it, such as young children or people with aphasia. In other words, the technology is in early stages, and the ultimate clinical applications are still in question, but this could still be a large advance in the study and control of pain.

The gap between something as small as DNA molecules and something as complex as speech and language seems so large at first glimpse as to be unbridgeable. The gap can be filled, but it is not straightforward.

Genes generally encode proteins, which have different functions depending on their shape. Proteins are the machinery that make cells like neurons work. Neurons form neural circuits, networks that have functions such as speech, language, and hearing. To understand how genes impact language, work has to be done on all these different levels.

At the Cognitive Neurology Society's 2013 Annual Meeting in San Francisco, Dr. Simon Fisher described a family of 15 people, all of whom had a severe disorder of speech. The family was found to have a mutation in a gene named FOXP2.

This single mutation alters one amino acid in a protein, which changes the ability of the protein to stick to part of DNA that otherwise would. Such a small difference completely alters the ability to use language. While this is very rare, it proves a point. A small genetic mutation can have large ramifications for our ability to communicate.

FOXP2 encodes a protein by the same name that serves as a transcription factor, meaning that it regulates how DNA is interpreted by the body. One of these regulated pieces of DNA is a gene named contactin associated protein 2 (CNTNAP2). If there is a lot of FOXP2 around, this gene is less expressed, resulting in less CNTNAP2. That's important, because CNTNAP2 has roles in neural development and in conducting electrical activity across the brain.

By collaborating with other researchers, 184 families with language impairment were studied, and they found that variants in this gene often had language problems, though they were sometimes milder than the original family. In an independent study, Dr. Dan Geschwind at UCSF found that one variant was also associated with delayed language in children with autism. It was also found to correlate with delayed language and to be related to some cases of dyslexia.

When looking at the level of neural networks, the researchers were able to rely on animal models. FOXP2 is found in many different animals, including mice. Looking at mice with similar mutations, the researchers found that the gene correlated with the number of connections formed between neurons. The neurite processes, branches that touch and share information, were shorter, and didn't branch as much in mutated mice. These mice with diminished FOXP2 function had significant problems learning motor skills.

All in all, researchers concluded that FOXP2 leads to rare coding mutations that can change language dramatically. A mutation in just CNTNAP2, though, is more common and increases the risk of less obvious language problems. Two little genes, but with big impact on language.

It used to be believed that the brain was done producing new cells by the time we reached adulthood. Now we've learned something more exciting-- our brain produces new neurons all the time. True, it only does so in certain areas, and doesn't do so very quickly, but nevertheless, these new cells have important functions in how we learn and develop.

Dr. Fred Gage of the Salk Institute was one of the first eeakers at the 20th annual meeting of the Cognitive Neuroscience Society. Dr. Salk discussed his research in neurogenesis.

In 1998, Dr. Salk showed how neurons develop from stem cells throughout a persons life. This primarily happens in the olfactory bulb, the hippocampus, and a region near the center of the brain called the subependymal zone. The hippocampus is particularly interesting, since this is the region responsible for forming memories.

Interestingly, the new nerve cells don't seem to form new networks, but replace older neurons, perhaps to allow for better functioning. In as little as two months, the new neurons become fully functional members of the hippocampus, specifically in a region called the dentate gyrus which helps us separate and process information prior to creating a memory. He also demonstrated that enriched environments can help animals to generate even more of these neurons. Even simple exercise can increase production by almost five times in rodents.

While those studies have just been done in rats, other studies, such as those done in London cab drivers, show that our own hippocampus also changes based on our learning and experience. This may have important ramifications in modern medicine. For example, having more ability to form new hippocampal neurons could help us resist the effects of the disorders like Alzheimer's disease. Maybe this is why research suggests that both exercise and mental activity can help protect against dementia.

One more reason for me to keep going to these conferences!