Trichotillomania is described as the recurrent pulling out of one’s own hair, leading to alone is and marked impairment. It is included under the OCD type disorders in the DSM-V. The other disorders now in that category include body dysmorphic disorder, hoarding disorder, excoriation disorder, and OCD. The lifetime prevalence is estimated at around .6% with a  F:M ratio of 4:1. The typical age of onset is between 10-13 years. The pulling can be automatic or focused. Over 20% of patients also experience trichophagia. Only 1/3 of patients with the disorder seek treatment. The disease is highly comorbidies with other psychiatric disorders, particularly those in the. OCD spectrum. Stimulants can make the pulling worse. It is also associated with rare variations in the SAPAP3 gene and does show a familial pattern. Treatments include psychotherapy, usually behavioral using habit reversal techniques (self monitoring, awareness training, competing response training, and stimulus control procedures) and pharmacotherapy (clomping mine, antipsychotic medications, and glutamate rigs agents). Among the glutamatergic agents, N-acetyl cysteine (NAC) has demonstrated benefit in a double blind PC trial…at a dosage of 200 mg. twice a day. Other agents worth noting include  olanzapine.  SSRIS have not yet shown to be that effective, adn fluvoxamine may be the drug of choice. 

Ketamine is a non competitive, N-methylfolate-D-aspartame glutamate receptor antagonist that is approved as an anesthetic agent. Recent studies have shown a rapid onset (2-24 hours post infusion) of antidepressant effect. This effect is short lived, with range of effect form 3-17 days. Studies have found twice weekly dosing to be sufficient over a 4-6  week period. The dose was .5mg/kg. Side effects included headache, dizziness, and nausea as well as acute transient psychotomimetic and dissociative symptoms which resolved within 2 hours. At this time, however studies over efficacy for longer time periods is needed. 

Now strategy for the treatment of treatment resistant depression has been the addition of anti-inflammatory agents, including COX-2 inhibitors, aspirin, and NSAIDS. Statins, used primarily for their lipid lowering properties also have direct anti-inflammatory effects. FIndings: concomitant use of an SSRi and a station was associated with a decreased risk for both psychiatric and general medical hospital contacts.  It was also NOT associated with increases in mortality. Over 870,000 patients were included in the study. 

It has been reported that almost 90% of people that abuse alcohol have sleep disturbances. other problems also exist for abuse of marijuana, cocaine, pain killers, caffeine, and nicotine.  Substance use leads to disruption in a number of neurotransmitters including acetylcholine, GABA, glutamate, norepinephrine, and orexin.

Alcohol can promote sleep but leads to fragmented restless sleep. There is also a decrease in total REM percentage and prolongation in REM onset latency. Alcohol also selectively inhibits motor activity in the upper airway with a corresponding increase in inspiratory resistance and snoring. Gabapentin and trazadone have shown some positive effects as sleep aids in patients with alcoholism. Trazadone has been the medication of choice to treat insomnia in early recovery for many years. Gabapentin is also relatively safe with few drug-drug interactions, low addictive potential, and no hepatic metabolism. It is known to increase cerebral concentrations of the inhibitory neurotransmitter GABA and is involved in the modulation of glutamate and norepinephrine. Rozarem can be of help by acting as an agonist at melatonin receptor and increasing total sleep time and decreasing sleep onset latency.

Marijuana with chronic use can lead to a reduction in stage N3 and decreased total sleep time. IT can also lead to decrease in REM percentage and prolongation or REM latency.

Nicotine causes longer sleep latency, decreased total sleep time, increased REM onset and decreased stage N3 sleep.

Yes, it is possible with certain medications that it can accelerate hair loss and we always must evaluate the  risk vs. benefits of treatment in these cases. But there are some over the counter things that work if the causative medication has been helpful with psychiatric symptoms.  For starters, one can try 200mcgs of selenium in combination with 50 mg of zinc. Nioxin shampoo has also been recommended as well as addition of rosemary and lavender to hair products.  5000mcgs Biotin has also been recommended. It is  important to make sure  hair loss is not caused by another underlying medical condition like hypothyroidism or as a side effect from oral contraceptive pills. If you are loosing hair, discuss this with your doctor as there are treatments.

Depression is affects approximately 350 million people worldwide, and approximately 7% of the US population. The primary objective is to treat to remission, and if they do not are considered to be treatment resistant. Resistance is often considered the failure of 2 adequate treatment trials. It is believed that approximately 45% of patients are treatment resistant, according to a major study. Risk factors for treatment resistance include psychiatric comorbidies, medical comorbidies, and genetic preponderance. 

If you are not responding to medication it is imperative to reevaluate diagnosis, complete an adequate trial of at least 4-6 weeks on a medication, and adhere to directions in taking medication. 

A recent retrospective review of close to 50,000 women, divided into 3 groups; never exposed to ssri’s and no psychiatric problem, having a psychiatric diagnosis (98% an affective disorder) but not taking an ssri, and having a psychiatric disorder and treating with an ssri..showed that treatment of the psychiatric disorder had a protective effect. The was significant as there was a lower risk of preterm birth and c sections. There however was a higher risk of neonatal problems as reported in prior studies. 

Folate is a vitamin, B9, needed by the body.  L Methyfolate is the active form of the vitamin. It helps to regulate the synthesis of serotonin, dopamine, and norepinephrine. 

A key regulatory enzyme, methylene tetrahydrofolate reductase (MTHFR), converts dietary folate to useable L methylfolate.

L methylfolate assists in the formation of a critical cofactor, known as tetrahydrobiopterin or BH4 which actives the enzymes that produce the neurotransmitters.

People at risk for low folate include abusers of alcohol, pregnant women, those suffering with an eating disorder, those with high homocysteine levels, and patients on lamictal or valproate which interfere with the conversion of dietary folate to L methylfolate. 
Patients on antidepressants that fail to respond, should consider augmentation with L methyfolate, as without it, the key neurotransmitters, which regulate mood, cannot be synthesized. 

Mant patients after a period of time on antidepressants develop considerable fatigue and apathy, described by a lack of motivation, energy and a feeling of  just “wanting to sit on the  couch.” 

What does this mean?

For starters it could represent a side effect of could represent a worsening of symptoms. 

What can be done?

1) decrease the dose to see if apathy or fatigue resolves

2) switch to dose in evening 

3) add a stimulant–bupropion, modafanil

4) change to a TCA not associated with apathy

5) add abilify

6) if insomnia develops with the antidepressant, adding trazodone or remeron for a more restful sleep may help

In review of the several studies, although most are case reports as we do not test medication on pregnant women revealed several areas of consistency.

1) there is a possible effect of antidepressants in precipitating. spontaneous abortion and miscarriage.

2) there is no effect seen associating use of antidepressants with fetal death

3) there is a possible association between paroxetine and cardiac malformations.

4) there is a likely effect of antidepressants on preterm birth.

5) there is a probable effect of antidepressant exposure and development of a neonatal behavioral syndrome.

But, none of the effects are large and serious consequences are rare.

use of antidepressants during pregnancy, is a risk vs. ratio decision. In addition, in reviewing the studies there is no way to avoid bias for depression and the risk of depressive symptoms on pregnancy.