Q. If a man has an underactive thyroid and is receiving treatment for it, has already gained weight, etc, does it affect his sex life in any way at all? If one has this condition as well as severed migraines, and is in their late 40's, would they be able to live a normal life or would they need nursing care?
A. Hypo-thyroidism can affect all aspects of life, generating a general "slowing down" all many bodily functions and the Basal Metabolic Rate. That does not necessarily mean it will, simply that it can. Treatment is simple, using replacement of the thyroid hormone normally produced by he gland a near-normal life can be expected. THE DOC

Q. How does one get rid of a toe nail that continues to grow split down the middle ?
A. Suggest a consulatiotion with a podiatrist: splintiong in place may help. THE DOC

Q. I have a question regarding pregnancy. If you have sexual intercourse a day or two before your period and then you do get you period, does that mean that you could still be pregnant? Also how effective is the morning after pill?
A. provided the period is normal in amount and duration, no. and the morning after pill is 75-80% effective as a guide

Q. I am investigating the possibility of an adult circumcision and am wondering if you have any information on the subject or could direct me to possible sources online. thanks.
A. Not much out here on this one in medical texts (???too political???)
These words from Harrisons Principles of Internal Medicine:
"Finally, lack of circumcision has been identified as a risk factor for urinary tract infection in both neonates and young men."
Check out this URL for more,a s part of the ANZWERS search engine:

Q. My daugher has been diagnosed with periventricular leukomalacia (bilateral). I am looking for any information that might be available.
If you have any suggestions on where to look, please let me know.
A. Without further information, we have sourced the folowing article which deals with lukoencephalopathy, the closest match we could come to leukomalacia. "Malacia" refers to a thinning of the tissue, in this case the white matter of the brain, and "peri-ventricular" to that tissue on either side of (both) ventricals of the brain (normal, fluid filled cavitits within the brain itself).
There is a possibility that the speciific diagnosis you ahve been given is quite a differenct disorde, in which the following discussion is npot applicable, but was the best we copuld do under the circumstances.

As the name implies, progressive multifocal leukoencephalopathy (PML) is a progressive disorder characterized pathologically by multifocal areas of demyelination, which vary greatly in size and are scattered throughout the CNS. In addition to demyelination, there are characteristic cytologic alterations in both astrocytes and oligodendrocytes. Astrocytes are tremendously enlarged and contain hyperchromatic, deformed, and bizarre nuclei and frequent mitotic figures. Oligodendrocytes have enlarged, densely staining nuclei that contain viral inclusions formed by crystalline arrays of JC virus particles. Patients often present with visual deficits (45 percent), typically a homonymous hemianopia, and mental impairment (38 percent) (dementia, confusion, personality change). Motor weakness may not be present early but eventually occurs in 75 percent of cases.
CT and MRI remain the most valuable diagnostic studies in suggesting the diagnosis of PML. CT shows hypodense nonenhancing white matter lesions without associated edema or mass effect. Lesions are typically located periventricularly, in the centrum semiovale, in the parietal-occipital region, and in the cerebellum. MRI is more sensitive than CT and reveals hyperintense signal in the white matter on T2-weighted spin-echo images. MRI shows multifocal asymmetric, coalescing white matter lesions with a predilection for the occipital and parietal lobes. These lesions are generally nonenhancing on T1-weighted images following administration of Gd-DTPA or related contrast agents. EEG almost always shows focal or diffuse slowing, and abnormalities may occasionally precede those seen by CT. The CSF is typically normal, although mild elevation in protein and/or IgG may be found. Pleocytosis occurs in less than 25 percent of cases, is predominantly mononuclear, and rarely exceeds 25 cells per microliter.
Recently, PCR amplification of JC virus DNA from CSF has shown promise as a diagnostic test for PML. The test has high specificity, but sensitivity has varied among studies. Rare cases of positive CSF PCR for JC virus DNA in the absence of clinical or radiographic evidence of PML have been described in HIV-infected patients. It remains to be established whether these results are false positive or are indicative of preclinical PML. The presence of oligoclonal bands, a substantial pleocytosis, or PMNs or red cells in the CSF should suggest such possibilities as acute multiple sclerosis, acute hemorrhagic leukoencephalitis, HIV-associated leukoencephalomyelopathy, multifocal VZV leukoencephalitis, or postinfectious or vaccinal immune-mediated encephalomyelitis.
Almost all patients (>95 percent) have an underlying immunosuppressive disorder. Prior to the HIV epidemic, common associated diseases included lymphoproliferative disorders, immune deficiency states, myeloproliferative disease, and chronic infectious or granulomatous diseases. Since 1984, the importance of these associated disorders has been dwarfed by that of AIDS.
According to some recent estimates, more than 60 percent of currently diagnosed PML cases occur in patients with AIDS. Conversely, it has been estimated that nearly 1 percent of AIDS patients will develop PML. Early indications suggest that the basic clinicopathologic features of AIDS-associated PML do not differ significantly from those of non-AIDS-associated PML. Some patients with AIDS-associated PML have shown significant spontaneous improvement in the absence of therapy.
Unfortunately, this appears to be the exception rather than the rule, and most cases pursue the same relentless downhill course to death that characterizes almost all reported cases of non-AIDS-associated PML. Definitive diagnosis depends on identification of the characteristic neuropathologic abnormalities at biopsy or necropsy. The presence of JC virus antigen and genomic DNA can be confirmed by immunocytochemistry, in situ hybridization, and PCR amplification on brain tissue. However, detection of JC virus antigen or genomic material is not diagnostic of PML unless accompanied by characteristic pathologic changes, since both antigen and genomic material can be found in the brains of normal patients. Between 80 and 90 percent of the population is seropositive for JC virus by middle adult life. Virus may remain latent in brain or other tissues and be reactivated during immunosuppression. PML also may result from primary exposure to JC virus in an immunocompromised host, since 10 to 20 percent of individuals are seronegative at the time of disease diagnosis. As discussed above, PCR amplification of JC virus DNA from CSF appears to be a promising new diagnostic tool.
No effective therapy for PML is currently available. Anecdotal reports have described clinical and radiographic stabilization and in some cases improvement in sporadic patients treated with intravenous or intrathecal cytarabine alone or in combination with a-interferon. A multicenter trial supported by the National Institutes of Health that compared antiretroviraltherapy alone to antiretroviral therapy plus either intravenous or intrathecal cytarabine in biopsy-documented HIV-associated PML failed to show any significant benefit from cytarabine treatment.