Norra MacReady

NEWPORT BEACH, CALIF. — The hands-down winner in the mosquito wars is DEET, but there are other ways of fighting off mosquitoes, according to two presentations at the annual meeting of the Pacific Dermatologic Association.

One approach is simply to avoid the things that attract the insects, said Tissa Hata, M.D., of the University of California, San Diego. At close range, mosquitoes rely heavily on olfactory cues and are drawn to floral fragrances in soaps, perfumes, and hair products. Dark clothing acts as a long-range attractant, and mosquitoes can detect carbon dioxide from breath and skin from a distance of 36 m. The combination of carbon dioxide and lactic acid is also a heady mix—if you're a mosquito.

The answer is to wear light-colored clothing, avoid fragrances, and “don't give off a lot of hot air,” she said.

A product containing 2% soybean oil did well in a comparison of mosquito repellants. Although a product with the highest concentration of DEET (N, N-diethyl-3-methylbenzamide) provided 301 minutes of protection, one with soybean oil warded off the bugs for 94 minutes. The oil can irritate children's eyes, so parents should not put it on their children's hands, Dr. Hata said. None of the other non-DEET products fared well in the comparison (N. Engl. J. Med. 2002; 347:13-18).

According to anecdotal reports, rubbing fabric softener sheets on the skin is effective, said Allan L. Kayne, M.D., a dermatologist with Berlex Pharmaceuticals in Montville, N.J. But he recommended that they not be used on infants or children.

He listed several other approaches anecdotally reported to be effective:

▸ Vick's VapoRub.

▸ A lotion that contains ethyl butylacetylaminopropionate (Skin-So-Soft Bug Guard made by Avon).

▸ Pure vanilla extract (not vanilla flavoring), mixed with equal parts water.

▸ Daily supplements of 100 mg thiamine.

▸ Cinnamon oil.

Other recommendations include avoiding bananas, which are thought to attract the insects, and planting marigolds, which contain pyrethrums that repel insects.

NEWPORT BEACH, CALIF. — The hands-down winner in the mosquito wars is DEET, but there are other ways of fighting off mosquitoes, according to two presentations at the annual meeting of the Pacific Dermatologic Association.

One approach is simply to avoid the things that attract the insects, said Tissa Hata, M.D., of the University of California, San Diego. At close range, mosquitoes rely heavily on olfactory cues and are drawn to floral fragrances in soaps, perfumes, and hair products. Dark clothing acts as a long-range attractant, and mosquitoes can detect carbon dioxide from breath and skin from a distance of 36 m. The combination of carbon dioxide and lactic acid is also a heady mix—if you're a mosquito.

The answer is to wear light-colored clothing, avoid fragrances, and “don't give off a lot of hot air,” she said.

A product containing 2% soybean oil did well in a comparison of mosquito repellants. Although a product with the highest concentration of DEET (N, N-diethyl-3-methylbenzamide) provided 301 minutes of protection, one with soybean oil warded off the bugs for 94 minutes. The oil can irritate children's eyes, so parents should not put it on their children's hands, Dr. Hata said. None of the other non-DEET products fared well in the comparison (N. Engl. J. Med. 2002; 347:13-18).

According to anecdotal reports, rubbing fabric softener sheets on the skin is effective, said Allan L. Kayne, M.D., a dermatologist with Berlex Pharmaceuticals in Montville, N.J. But he recommended that they not be used on infants or children.

He listed several other approaches anecdotally reported to be effective:

▸ Vick's VapoRub.

▸ A lotion that contains ethyl butylacetylaminopropionate (Skin-So-Soft Bug Guard made by Avon).

▸ Pure vanilla extract (not vanilla flavoring), mixed with equal parts water.

▸ Daily supplements of 100 mg thiamine.

▸ Cinnamon oil.

Other recommendations include avoiding bananas, which are thought to attract the insects, and planting marigolds, which contain pyrethrums that repel insects.

NEWPORT BEACH, CALIF. — The hands-down winner in the mosquito wars is DEET, but there are other ways of fighting off mosquitoes, according to two presentations at the annual meeting of the Pacific Dermatologic Association.

One approach is simply to avoid the things that attract the insects, said Tissa Hata, M.D., of the University of California, San Diego. At close range, mosquitoes rely heavily on olfactory cues and are drawn to floral fragrances in soaps, perfumes, and hair products. Dark clothing acts as a long-range attractant, and mosquitoes can detect carbon dioxide from breath and skin from a distance of 36 m. The combination of carbon dioxide and lactic acid is also a heady mix—if you're a mosquito.

The answer is to wear light-colored clothing, avoid fragrances, and “don't give off a lot of hot air,” she said.

A product containing 2% soybean oil did well in a comparison of mosquito repellants. Although a product with the highest concentration of DEET (N, N-diethyl-3-methylbenzamide) provided 301 minutes of protection, one with soybean oil warded off the bugs for 94 minutes. The oil can irritate children's eyes, so parents should not put it on their children's hands, Dr. Hata said. None of the other non-DEET products fared well in the comparison (N. Engl. J. Med. 2002; 347:13-18).

According to anecdotal reports, rubbing fabric softener sheets on the skin is effective, said Allan L. Kayne, M.D., a dermatologist with Berlex Pharmaceuticals in Montville, N.J. But he recommended that they not be used on infants or children.

He listed several other approaches anecdotally reported to be effective:

▸ Vick's VapoRub.

▸ A lotion that contains ethyl butylacetylaminopropionate (Skin-So-Soft Bug Guard made by Avon).

▸ Pure vanilla extract (not vanilla flavoring), mixed with equal parts water.

▸ Daily supplements of 100 mg thiamine.

▸ Cinnamon oil.

Other recommendations include avoiding bananas, which are thought to attract the insects, and planting marigolds, which contain pyrethrums that repel insects.

NEWPORT BEACH, CALIF. — Tinea capitis is the most common dermatophytic infection of childhood, Sheila Fallon Friedlander, M.D., said at the annual meeting of the Pacific Dermatologic Association.

She answered some pediatricians' and family physicians' questions about the condition:

▸ Which organisms are most likely to cause tinea capitis? In the United States, Trichophyton tonsurans accounts for most cases, said Dr. Friedlander, a pediatric dermatologist at the University of California, San Diego. Microsporum canis is occasionally seen, and usually is transmitted from a household pet.

However, in other countries, other organisms may cause tinea capitis, which is something to keep in mind when examining a child who immigrated from abroad or who was adopted from a foreign country.

▸ What is the treatment of choice? Treatment should consist of oral griseofulvin plus a topical antifungal agent. Dr. Friedlander recommends starting griseofulvin at a dose of 20 mg/kg, which is higher than the standard dose but produces the best cure rates. A lower dose is “an inappropriate treatment for tinea capitis,” she said.

Evidence is accumulating that terbinafine (Lamisil), given at 3-6 mg/kg, is as safe and effective as griseofulvin and acts within 2 weeks.

Enhanced efficacy has been seen with higher dosing of terbinafine in the range of 5-8 mg/kg per day.

Some studies have documented good response rates with itraconazole (Sporanox) and fluconazole (Diflucan).

▸ How long should treatment last? In her practice, Dr. Friedlander usually treats for 8 weeks. Many experts recommend treating until 2 weeks after resolution of symptoms, which may require weeks to months of therapy.

▸ What do you tell parents about griseofulvin? Griseofulvin is inexpensive and has a long track record of efficacy. It is a relatively safe drug, but about 30% of patients develop side effects that include headache, gastrointestinal upset, and photosensitivity.

▸ Are laboratory tests necessary? Lab tests are needed only if the patient requires more than 8 weeks of treatment.

▸ Do you treat the entire family? Ask about other family members and treat them if they are symptomatic. T. tonsurans is commonly passed among wrestlers. Infection with M. canis should lead to questions about the family pet, as cats and dogs frequently harbor these organisms.

Some family members may insist on treatment even when they are asymptomatic. Dr. Friedlander prescribes topical therapy to reassure them.

▸ Do you prescribe prednisone for kerions? Most patients don't need prednisone. Kerions (nodular, exudative, circumscribed tumefactions covered with pustules) usually respond to systemic antifungal therapy. “We recommend adjunctive topical antifungal therapy, but rarely utilize the systemic therapy, Dr. Friedlander said.

If the patient doesn't improve within 2 weeks, Dr. Friedlander said she will add systemic therapy, but in most cases that is not necessary.

NEWPORT BEACH, CALIF. — Tinea capitis is the most common dermatophytic infection of childhood, Sheila Fallon Friedlander, M.D., said at the annual meeting of the Pacific Dermatologic Association.

She answered some pediatricians' and family physicians' questions about the condition:

▸ Which organisms are most likely to cause tinea capitis? In the United States, Trichophyton tonsurans accounts for most cases, said Dr. Friedlander, a pediatric dermatologist at the University of California, San Diego. Microsporum canis is occasionally seen, and usually is transmitted from a household pet.

However, in other countries, other organisms may cause tinea capitis, which is something to keep in mind when examining a child who immigrated from abroad or who was adopted from a foreign country.

▸ What is the treatment of choice? Treatment should consist of oral griseofulvin plus a topical antifungal agent. Dr. Friedlander recommends starting griseofulvin at a dose of 20 mg/kg, which is higher than the standard dose but produces the best cure rates. A lower dose is “an inappropriate treatment for tinea capitis,” she said.

Evidence is accumulating that terbinafine (Lamisil), given at 3-6 mg/kg, is as safe and effective as griseofulvin and acts within 2 weeks.

Enhanced efficacy has been seen with higher dosing of terbinafine in the range of 5-8 mg/kg per day.

Some studies have documented good response rates with itraconazole (Sporanox) and fluconazole (Diflucan).

▸ How long should treatment last? In her practice, Dr. Friedlander usually treats for 8 weeks. Many experts recommend treating until 2 weeks after resolution of symptoms, which may require weeks to months of therapy.

▸ What do you tell parents about griseofulvin? Griseofulvin is inexpensive and has a long track record of efficacy. It is a relatively safe drug, but about 30% of patients develop side effects that include headache, gastrointestinal upset, and photosensitivity.

▸ Are laboratory tests necessary? Lab tests are needed only if the patient requires more than 8 weeks of treatment.

▸ Do you treat the entire family? Ask about other family members and treat them if they are symptomatic. T. tonsurans is commonly passed among wrestlers. Infection with M. canis should lead to questions about the family pet, as cats and dogs frequently harbor these organisms.

Some family members may insist on treatment even when they are asymptomatic. Dr. Friedlander prescribes topical therapy to reassure them.

▸ Do you prescribe prednisone for kerions? Most patients don't need prednisone. Kerions (nodular, exudative, circumscribed tumefactions covered with pustules) usually respond to systemic antifungal therapy. “We recommend adjunctive topical antifungal therapy, but rarely utilize the systemic therapy, Dr. Friedlander said.

If the patient doesn't improve within 2 weeks, Dr. Friedlander said she will add systemic therapy, but in most cases that is not necessary.

NEWPORT BEACH, CALIF. — Tinea capitis is the most common dermatophytic infection of childhood, Sheila Fallon Friedlander, M.D., said at the annual meeting of the Pacific Dermatologic Association.

She answered some pediatricians' and family physicians' questions about the condition:

▸ Which organisms are most likely to cause tinea capitis? In the United States, Trichophyton tonsurans accounts for most cases, said Dr. Friedlander, a pediatric dermatologist at the University of California, San Diego. Microsporum canis is occasionally seen, and usually is transmitted from a household pet.

However, in other countries, other organisms may cause tinea capitis, which is something to keep in mind when examining a child who immigrated from abroad or who was adopted from a foreign country.

▸ What is the treatment of choice? Treatment should consist of oral griseofulvin plus a topical antifungal agent. Dr. Friedlander recommends starting griseofulvin at a dose of 20 mg/kg, which is higher than the standard dose but produces the best cure rates. A lower dose is “an inappropriate treatment for tinea capitis,” she said.

Evidence is accumulating that terbinafine (Lamisil), given at 3-6 mg/kg, is as safe and effective as griseofulvin and acts within 2 weeks.

Enhanced efficacy has been seen with higher dosing of terbinafine in the range of 5-8 mg/kg per day.

Some studies have documented good response rates with itraconazole (Sporanox) and fluconazole (Diflucan).

▸ How long should treatment last? In her practice, Dr. Friedlander usually treats for 8 weeks. Many experts recommend treating until 2 weeks after resolution of symptoms, which may require weeks to months of therapy.

▸ What do you tell parents about griseofulvin? Griseofulvin is inexpensive and has a long track record of efficacy. It is a relatively safe drug, but about 30% of patients develop side effects that include headache, gastrointestinal upset, and photosensitivity.

▸ Are laboratory tests necessary? Lab tests are needed only if the patient requires more than 8 weeks of treatment.

▸ Do you treat the entire family? Ask about other family members and treat them if they are symptomatic. T. tonsurans is commonly passed among wrestlers. Infection with M. canis should lead to questions about the family pet, as cats and dogs frequently harbor these organisms.

Some family members may insist on treatment even when they are asymptomatic. Dr. Friedlander prescribes topical therapy to reassure them.

▸ Do you prescribe prednisone for kerions? Most patients don't need prednisone. Kerions (nodular, exudative, circumscribed tumefactions covered with pustules) usually respond to systemic antifungal therapy. “We recommend adjunctive topical antifungal therapy, but rarely utilize the systemic therapy, Dr. Friedlander said.

If the patient doesn't improve within 2 weeks, Dr. Friedlander said she will add systemic therapy, but in most cases that is not necessary.

LAS VEGAS – Hallucinations are a significant predictor of functional impairment in patients with Alzheimer's disease, Wing Yee Mok, M.D., said at the annual meeting of the American Geriatrics Society.

In a retrospective analysis of 100 patients at a mean age of 80 years and with a mean 3 years of education, the presence of hallucinations, as well as a low score on the Mini-Mental State Examination (MMSE), were independent predictors of problems in activities of daily living, said Dr. Mok, a resident in the department of medicine at Queen Mary Hospital in Hong Kong.

Cognitive impairment is known to affect functional capacity, but the impact of noncognitive symptoms, such as hallucinations, has not been studied as extensively, she said.

The patients were recruited from the memory clinic at Queen Mary Hospital. They underwent a series of tests to assess various aspects of their cognitive and functional abilities, including the MMSE, the Barthel Index of Activities of Daily Living (BADL), and Lawton's Instrumental Activities of Daily Living (IADL). They were also examined for noncognitive psychiatric symptoms, including hallucinations, delusions, anxiety, euphoria, and apathy.

The BADL measures the patient's ability to perform basic daily activities, such as bathing, eating, and grooming without assistance. Scores range from 0, suggesting complete incapacitation, to 20, complete independence. The patients in this study had a mean score of 18.4.

The IADL assesses the patient's ability to perform tasks that require some planning and abstraction, such as doing laundry, shopping for groceries, and managing money. Scores range from 0, suggesting inability to perform the task at all, to 8, meaning no help is needed with any of the activities. These patients had a mean score of 5.9.

The MMSE measures cognitive function by asking patients the date and place, having them name various objects, remember words, and subtract a series of numbers. Scores vary depending on the patient's age and level of education, but mean scores for unimpaired 80-year-olds range from 20, for those with up to a fourth-grade education, to 27, for those with a college degree. The mean MMSE score for these patients was 15.1.

In a multiple linear regression analysis, the presence of hallucinations was a significant independent predictor of impairment as measured by the IADL but not the BADL. A low score on the MMSE correlated strongly with low scores on the BADL and the IADL and was another independent predictor of poor functional status.

Screening for and managing hallucinations could improve functional status in this patient population, Dr. Mok said.

LAS VEGAS – Hallucinations are a significant predictor of functional impairment in patients with Alzheimer's disease, Wing Yee Mok, M.D., said at the annual meeting of the American Geriatrics Society.

In a retrospective analysis of 100 patients at a mean age of 80 years and with a mean 3 years of education, the presence of hallucinations, as well as a low score on the Mini-Mental State Examination (MMSE), were independent predictors of problems in activities of daily living, said Dr. Mok, a resident in the department of medicine at Queen Mary Hospital in Hong Kong.

Cognitive impairment is known to affect functional capacity, but the impact of noncognitive symptoms, such as hallucinations, has not been studied as extensively, she said.

The patients were recruited from the memory clinic at Queen Mary Hospital. They underwent a series of tests to assess various aspects of their cognitive and functional abilities, including the MMSE, the Barthel Index of Activities of Daily Living (BADL), and Lawton's Instrumental Activities of Daily Living (IADL). They were also examined for noncognitive psychiatric symptoms, including hallucinations, delusions, anxiety, euphoria, and apathy.

The BADL measures the patient's ability to perform basic daily activities, such as bathing, eating, and grooming without assistance. Scores range from 0, suggesting complete incapacitation, to 20, complete independence. The patients in this study had a mean score of 18.4.

The IADL assesses the patient's ability to perform tasks that require some planning and abstraction, such as doing laundry, shopping for groceries, and managing money. Scores range from 0, suggesting inability to perform the task at all, to 8, meaning no help is needed with any of the activities. These patients had a mean score of 5.9.

The MMSE measures cognitive function by asking patients the date and place, having them name various objects, remember words, and subtract a series of numbers. Scores vary depending on the patient's age and level of education, but mean scores for unimpaired 80-year-olds range from 20, for those with up to a fourth-grade education, to 27, for those with a college degree. The mean MMSE score for these patients was 15.1.

In a multiple linear regression analysis, the presence of hallucinations was a significant independent predictor of impairment as measured by the IADL but not the BADL. A low score on the MMSE correlated strongly with low scores on the BADL and the IADL and was another independent predictor of poor functional status.

Screening for and managing hallucinations could improve functional status in this patient population, Dr. Mok said.

LAS VEGAS – Hallucinations are a significant predictor of functional impairment in patients with Alzheimer's disease, Wing Yee Mok, M.D., said at the annual meeting of the American Geriatrics Society.

In a retrospective analysis of 100 patients at a mean age of 80 years and with a mean 3 years of education, the presence of hallucinations, as well as a low score on the Mini-Mental State Examination (MMSE), were independent predictors of problems in activities of daily living, said Dr. Mok, a resident in the department of medicine at Queen Mary Hospital in Hong Kong.

Cognitive impairment is known to affect functional capacity, but the impact of noncognitive symptoms, such as hallucinations, has not been studied as extensively, she said.

The patients were recruited from the memory clinic at Queen Mary Hospital. They underwent a series of tests to assess various aspects of their cognitive and functional abilities, including the MMSE, the Barthel Index of Activities of Daily Living (BADL), and Lawton's Instrumental Activities of Daily Living (IADL). They were also examined for noncognitive psychiatric symptoms, including hallucinations, delusions, anxiety, euphoria, and apathy.

The BADL measures the patient's ability to perform basic daily activities, such as bathing, eating, and grooming without assistance. Scores range from 0, suggesting complete incapacitation, to 20, complete independence. The patients in this study had a mean score of 18.4.

The IADL assesses the patient's ability to perform tasks that require some planning and abstraction, such as doing laundry, shopping for groceries, and managing money. Scores range from 0, suggesting inability to perform the task at all, to 8, meaning no help is needed with any of the activities. These patients had a mean score of 5.9.

The MMSE measures cognitive function by asking patients the date and place, having them name various objects, remember words, and subtract a series of numbers. Scores vary depending on the patient's age and level of education, but mean scores for unimpaired 80-year-olds range from 20, for those with up to a fourth-grade education, to 27, for those with a college degree. The mean MMSE score for these patients was 15.1.

In a multiple linear regression analysis, the presence of hallucinations was a significant independent predictor of impairment as measured by the IADL but not the BADL. A low score on the MMSE correlated strongly with low scores on the BADL and the IADL and was another independent predictor of poor functional status.

Screening for and managing hallucinations could improve functional status in this patient population, Dr. Mok said.

IRVINE, CALIF. – Children with autism and pervasive developmental disorder show abnormalities in brain structure and chemistry early in their clinical course, Seth Friedman, Ph.D., said at the annual conference of the EEG and Clinical Neuroscience Society.

Brain-volume increases in autism are likely not present at birth but begin to develop in infancy, grow most marked by 3-4 years of age, and level off somewhat by age 6-7 years, a theory championed by Eric Courchesne, Ph.D., of the University of California, San Diego. These changes may reflect deficits in cortical volume and organization relative to that seen in children who are developing more typically, said Dr. Friedman, of the University of Washington, Seattle.

With his colleagues, Dr. Friedman compared magnetic resonance images from 45 children with autism or pervasive developmental disorder not otherwise specified (PDD-NOS) and from 14 children with other types of developmental delays (DD) with images from 26 typically developing (TD) children. All subjects were 3-4 years old.

The children in the autistic and PDD-NOS groups had significantly larger cerebral volumes than the other two groups. Their cerebellar, amygdala, and hippocampal volumes were also larger but were proportionate to the overall increase in cerebral size. However, the amygdala was disproportionately large in a subgroup of children with strictly defined autism. The findings were generally similar for boys and girls. Children with DD had smaller amygdalas (Neurology 2002;59:184-92).

Consistent with the findings of other studies, larger-than-average brains in the University of Washington autism sample leveled off in size over time, Dr. Friedman said. Some researchers have suggested that this early increase might be caused by a large number of neurons densely packed into the cortex.

To test this hypothesis, he and his associates evaluated regional brain chemistry in the same 45 children with autism and PDD-NOS, as well as 15 children with DD (the original 14 plus 1 more), and 13 of the original children in the TD group.

They used dual-proton echoplanar spectroscopic imaging to measure brain metabolite concentrations. They also measured each metabolite's relaxation time–the approximate time it takes a chemical system to return to its original state after being perturbed by an outside force, such as a change in temperature, pressure, or–in the case of magnetic resonance–radio waves. In this study, the relative measures of transverse relaxation (T2r) were calculated from the paired echoes to provide a picture of the metabolic activity within the subjects' gray matter.

Compared with the TD children, those with autism and PDD-NOS had T2r values of myoinositol, N-acetylaspartate, and creatine that were 13%, 10%, and 8% lower, respectively. These significant differences suggest there is a lower concentration of these metabolites in the gray matter. However, compared with those of the DD subjects, their T2r values for choline and creatine were 10% and 9% higher, respectively (Neurology 2003;60:100-7).

These data contradict the idea that people with autism experience dense neuronal packing early in the life, Dr. Friedman said. They may support a theory advanced by Manuel F. Casanova, M.D., of the University of Louisville (Ky.), that cortical minicolumns, self-contained organizational neuronal units found throughout the brain, are more numerous but smaller and less organized in these patients.

IRVINE, CALIF. – Children with autism and pervasive developmental disorder show abnormalities in brain structure and chemistry early in their clinical course, Seth Friedman, Ph.D., said at the annual conference of the EEG and Clinical Neuroscience Society.

Brain-volume increases in autism are likely not present at birth but begin to develop in infancy, grow most marked by 3-4 years of age, and level off somewhat by age 6-7 years, a theory championed by Eric Courchesne, Ph.D., of the University of California, San Diego. These changes may reflect deficits in cortical volume and organization relative to that seen in children who are developing more typically, said Dr. Friedman, of the University of Washington, Seattle.

With his colleagues, Dr. Friedman compared magnetic resonance images from 45 children with autism or pervasive developmental disorder not otherwise specified (PDD-NOS) and from 14 children with other types of developmental delays (DD) with images from 26 typically developing (TD) children. All subjects were 3-4 years old.

The children in the autistic and PDD-NOS groups had significantly larger cerebral volumes than the other two groups. Their cerebellar, amygdala, and hippocampal volumes were also larger but were proportionate to the overall increase in cerebral size. However, the amygdala was disproportionately large in a subgroup of children with strictly defined autism. The findings were generally similar for boys and girls. Children with DD had smaller amygdalas (Neurology 2002;59:184-92).

Consistent with the findings of other studies, larger-than-average brains in the University of Washington autism sample leveled off in size over time, Dr. Friedman said. Some researchers have suggested that this early increase might be caused by a large number of neurons densely packed into the cortex.

To test this hypothesis, he and his associates evaluated regional brain chemistry in the same 45 children with autism and PDD-NOS, as well as 15 children with DD (the original 14 plus 1 more), and 13 of the original children in the TD group.

They used dual-proton echoplanar spectroscopic imaging to measure brain metabolite concentrations. They also measured each metabolite's relaxation time–the approximate time it takes a chemical system to return to its original state after being perturbed by an outside force, such as a change in temperature, pressure, or–in the case of magnetic resonance–radio waves. In this study, the relative measures of transverse relaxation (T2r) were calculated from the paired echoes to provide a picture of the metabolic activity within the subjects' gray matter.

Compared with the TD children, those with autism and PDD-NOS had T2r values of myoinositol, N-acetylaspartate, and creatine that were 13%, 10%, and 8% lower, respectively. These significant differences suggest there is a lower concentration of these metabolites in the gray matter. However, compared with those of the DD subjects, their T2r values for choline and creatine were 10% and 9% higher, respectively (Neurology 2003;60:100-7).

These data contradict the idea that people with autism experience dense neuronal packing early in the life, Dr. Friedman said. They may support a theory advanced by Manuel F. Casanova, M.D., of the University of Louisville (Ky.), that cortical minicolumns, self-contained organizational neuronal units found throughout the brain, are more numerous but smaller and less organized in these patients.

IRVINE, CALIF. – Children with autism and pervasive developmental disorder show abnormalities in brain structure and chemistry early in their clinical course, Seth Friedman, Ph.D., said at the annual conference of the EEG and Clinical Neuroscience Society.

Brain-volume increases in autism are likely not present at birth but begin to develop in infancy, grow most marked by 3-4 years of age, and level off somewhat by age 6-7 years, a theory championed by Eric Courchesne, Ph.D., of the University of California, San Diego. These changes may reflect deficits in cortical volume and organization relative to that seen in children who are developing more typically, said Dr. Friedman, of the University of Washington, Seattle.

With his colleagues, Dr. Friedman compared magnetic resonance images from 45 children with autism or pervasive developmental disorder not otherwise specified (PDD-NOS) and from 14 children with other types of developmental delays (DD) with images from 26 typically developing (TD) children. All subjects were 3-4 years old.

The children in the autistic and PDD-NOS groups had significantly larger cerebral volumes than the other two groups. Their cerebellar, amygdala, and hippocampal volumes were also larger but were proportionate to the overall increase in cerebral size. However, the amygdala was disproportionately large in a subgroup of children with strictly defined autism. The findings were generally similar for boys and girls. Children with DD had smaller amygdalas (Neurology 2002;59:184-92).

Consistent with the findings of other studies, larger-than-average brains in the University of Washington autism sample leveled off in size over time, Dr. Friedman said. Some researchers have suggested that this early increase might be caused by a large number of neurons densely packed into the cortex.

To test this hypothesis, he and his associates evaluated regional brain chemistry in the same 45 children with autism and PDD-NOS, as well as 15 children with DD (the original 14 plus 1 more), and 13 of the original children in the TD group.

They used dual-proton echoplanar spectroscopic imaging to measure brain metabolite concentrations. They also measured each metabolite's relaxation time–the approximate time it takes a chemical system to return to its original state after being perturbed by an outside force, such as a change in temperature, pressure, or–in the case of magnetic resonance–radio waves. In this study, the relative measures of transverse relaxation (T2r) were calculated from the paired echoes to provide a picture of the metabolic activity within the subjects' gray matter.

Compared with the TD children, those with autism and PDD-NOS had T2r values of myoinositol, N-acetylaspartate, and creatine that were 13%, 10%, and 8% lower, respectively. These significant differences suggest there is a lower concentration of these metabolites in the gray matter. However, compared with those of the DD subjects, their T2r values for choline and creatine were 10% and 9% higher, respectively (Neurology 2003;60:100-7).

These data contradict the idea that people with autism experience dense neuronal packing early in the life, Dr. Friedman said. They may support a theory advanced by Manuel F. Casanova, M.D., of the University of Louisville (Ky.), that cortical minicolumns, self-contained organizational neuronal units found throughout the brain, are more numerous but smaller and less organized in these patients.

SAN FRANCISCO – Deep brain stimulation of the anterior thalamic nuclei shows promise in the management of epileptic seizures, judging from the findings of a small pilot study, Robert Fisher, M.D., said at the annual meeting of the Congress of Neurological Surgeons.

If further research results confirm the procedure's initial promise, deep brain stimulation could become one of a group of targeted therapies, he said.

That group of therapies includes radiation and local drug perfusion, which control severe epileptic seizures, said Dr. Fisher, who is professor of neurology at Stanford (Calif.) University.

The study population consisted of seven men and seven women, 19–44 years old, with partial and apparently generalized tonicoclonic seizures originating in the temporofrontal lobes and from multifocal regions.

Treatment efficacy was expressed in terms of responder rate, defined as the percentage of patients who experienced a decline of 50% or more in the number of seizures after deep brain stimulation.

By that criterion, the responder rate was 57% as long as 12 months post procedure, he reported.

Improvement was especially dramatic in four of five patients whose seizures were severe enough to make them fall down.

There was no control group in the study. However, these findings compare favorably with data that come from controlled clinical trials that involved gabapentin and lamotrigine in which responder rates were only 15%-20% among patients who were taking the drugs, Dr. Fisher pointed out.

One concern about deep brain stimulation is that it may inhibit neurologic activity at seizure foci but stimulate activity in surrounding areas of the brain.

“We will have to watch for that as we move forward,” he said.

A controlled, multicenter trial is now underway.

SAN FRANCISCO – Deep brain stimulation of the anterior thalamic nuclei shows promise in the management of epileptic seizures, judging from the findings of a small pilot study, Robert Fisher, M.D., said at the annual meeting of the Congress of Neurological Surgeons.

If further research results confirm the procedure's initial promise, deep brain stimulation could become one of a group of targeted therapies, he said.

That group of therapies includes radiation and local drug perfusion, which control severe epileptic seizures, said Dr. Fisher, who is professor of neurology at Stanford (Calif.) University.

The study population consisted of seven men and seven women, 19–44 years old, with partial and apparently generalized tonicoclonic seizures originating in the temporofrontal lobes and from multifocal regions.

Treatment efficacy was expressed in terms of responder rate, defined as the percentage of patients who experienced a decline of 50% or more in the number of seizures after deep brain stimulation.

By that criterion, the responder rate was 57% as long as 12 months post procedure, he reported.

Improvement was especially dramatic in four of five patients whose seizures were severe enough to make them fall down.

There was no control group in the study. However, these findings compare favorably with data that come from controlled clinical trials that involved gabapentin and lamotrigine in which responder rates were only 15%-20% among patients who were taking the drugs, Dr. Fisher pointed out.

One concern about deep brain stimulation is that it may inhibit neurologic activity at seizure foci but stimulate activity in surrounding areas of the brain.

“We will have to watch for that as we move forward,” he said.

A controlled, multicenter trial is now underway.

SAN FRANCISCO – Deep brain stimulation of the anterior thalamic nuclei shows promise in the management of epileptic seizures, judging from the findings of a small pilot study, Robert Fisher, M.D., said at the annual meeting of the Congress of Neurological Surgeons.

If further research results confirm the procedure's initial promise, deep brain stimulation could become one of a group of targeted therapies, he said.

That group of therapies includes radiation and local drug perfusion, which control severe epileptic seizures, said Dr. Fisher, who is professor of neurology at Stanford (Calif.) University.

The study population consisted of seven men and seven women, 19–44 years old, with partial and apparently generalized tonicoclonic seizures originating in the temporofrontal lobes and from multifocal regions.

Treatment efficacy was expressed in terms of responder rate, defined as the percentage of patients who experienced a decline of 50% or more in the number of seizures after deep brain stimulation.

By that criterion, the responder rate was 57% as long as 12 months post procedure, he reported.

Improvement was especially dramatic in four of five patients whose seizures were severe enough to make them fall down.

There was no control group in the study. However, these findings compare favorably with data that come from controlled clinical trials that involved gabapentin and lamotrigine in which responder rates were only 15%-20% among patients who were taking the drugs, Dr. Fisher pointed out.

One concern about deep brain stimulation is that it may inhibit neurologic activity at seizure foci but stimulate activity in surrounding areas of the brain.

“We will have to watch for that as we move forward,” he said.

A controlled, multicenter trial is now underway.

SAN FRANCISCO — The number of hospitals at which external carotid to internal carotid bypass procedures are performed is increasing, but so is associated mortality, Sepideh Amin-Hanjani, M.D., said at the annual meeting of the Congress of Neurological Surgeons.

Growth of external carotid to internal carotid (EC-IC) bypass procedures is greatest at low-volume centers and among inexperienced surgeons, said Dr. Amin-Hanjani, of Harvard Medical School, Boston.

In an analysis of 558 operations performed at 158 American hospitals by 145 surgeons between 1992 and 2001, the annual number of admissions for EC-IC bypass almost doubled from 190 per year from 1992 to 1996, to 360 per year from 1997 to 2001. Mortality more than doubled, from 2.5% to 5.9%, Dr. Amin-Hanjani said.

The median numbers of procedures per hospital and per surgeon were 3 and 2, respectively, over the decade. For 29% of patients, their EC-IC bypass was the only one recorded at the hospital for the year, and for 42% of patients, their surgeon performed no other EC-IC bypass.

Cerebral ischemia was the indication in 74% of procedures, followed by unruptured aneurysms (19%), and ruptured aneurysms (7%). Mortality was highest (21%) in patients with ruptured aneurysms, followed by those with unruptured aneurysms (7.7%), and cerebral ischemia (2.4%).

These findings were based on data from the Healthcare Cost and Utilization Project's third Nationwide Inpatient Sample.

“This technically demanding procedure has become a very low-volume operation at nearly all U.S. centers,” Dr. Amin-Hanjani said. Surgeons need experience with at least 20-30 cases to achieve patency rates of 90%-100%.

SAN FRANCISCO — The number of hospitals at which external carotid to internal carotid bypass procedures are performed is increasing, but so is associated mortality, Sepideh Amin-Hanjani, M.D., said at the annual meeting of the Congress of Neurological Surgeons.

Growth of external carotid to internal carotid (EC-IC) bypass procedures is greatest at low-volume centers and among inexperienced surgeons, said Dr. Amin-Hanjani, of Harvard Medical School, Boston.

In an analysis of 558 operations performed at 158 American hospitals by 145 surgeons between 1992 and 2001, the annual number of admissions for EC-IC bypass almost doubled from 190 per year from 1992 to 1996, to 360 per year from 1997 to 2001. Mortality more than doubled, from 2.5% to 5.9%, Dr. Amin-Hanjani said.

The median numbers of procedures per hospital and per surgeon were 3 and 2, respectively, over the decade. For 29% of patients, their EC-IC bypass was the only one recorded at the hospital for the year, and for 42% of patients, their surgeon performed no other EC-IC bypass.

Cerebral ischemia was the indication in 74% of procedures, followed by unruptured aneurysms (19%), and ruptured aneurysms (7%). Mortality was highest (21%) in patients with ruptured aneurysms, followed by those with unruptured aneurysms (7.7%), and cerebral ischemia (2.4%).

These findings were based on data from the Healthcare Cost and Utilization Project's third Nationwide Inpatient Sample.

“This technically demanding procedure has become a very low-volume operation at nearly all U.S. centers,” Dr. Amin-Hanjani said. Surgeons need experience with at least 20-30 cases to achieve patency rates of 90%-100%.

SAN FRANCISCO — The number of hospitals at which external carotid to internal carotid bypass procedures are performed is increasing, but so is associated mortality, Sepideh Amin-Hanjani, M.D., said at the annual meeting of the Congress of Neurological Surgeons.

Growth of external carotid to internal carotid (EC-IC) bypass procedures is greatest at low-volume centers and among inexperienced surgeons, said Dr. Amin-Hanjani, of Harvard Medical School, Boston.

In an analysis of 558 operations performed at 158 American hospitals by 145 surgeons between 1992 and 2001, the annual number of admissions for EC-IC bypass almost doubled from 190 per year from 1992 to 1996, to 360 per year from 1997 to 2001. Mortality more than doubled, from 2.5% to 5.9%, Dr. Amin-Hanjani said.

The median numbers of procedures per hospital and per surgeon were 3 and 2, respectively, over the decade. For 29% of patients, their EC-IC bypass was the only one recorded at the hospital for the year, and for 42% of patients, their surgeon performed no other EC-IC bypass.

Cerebral ischemia was the indication in 74% of procedures, followed by unruptured aneurysms (19%), and ruptured aneurysms (7%). Mortality was highest (21%) in patients with ruptured aneurysms, followed by those with unruptured aneurysms (7.7%), and cerebral ischemia (2.4%).

These findings were based on data from the Healthcare Cost and Utilization Project's third Nationwide Inpatient Sample.

“This technically demanding procedure has become a very low-volume operation at nearly all U.S. centers,” Dr. Amin-Hanjani said. Surgeons need experience with at least 20-30 cases to achieve patency rates of 90%-100%.

IRVINE, CALIF. — Children with autism and pervasive developmental disorder show abnormalities in brain structure and chemistry early in their life, Seth Friedman, Ph.D., said at the annual conference of the EEG and Clinical Neuroscience Society.

Brain-volume increases in autism are likely not present at birth but begin to develop in infancy, grow most marked by 3–4 years of age, and level off somewhat by age 6–7 years, a theory championed by Eric Courchesne, Ph.D., of the University of California, San Diego. These changes may reflect deficits in cortical volume and organization relative to that seen in children who are developing more typically, said Dr. Friedman, of the University of Washington, Seattle.

With his colleagues, Dr. Friedman compared magnetic resonance images from 45 children with autism or pervasive developmental disorder not otherwise specified (PDD-NOS) and from 14 children with other types of developmental delays (DD) with images from 26 typically developing (TD) children. All subjects were 3–4 years old.

The children in the autistic and PDD-NOS groups had significantly larger cerebral volumes than the other two groups. Their cerebellar, amygdala, and hippocampal volumes were also larger but were proportionate to the overall increase in cerebral size. However, the amygdala was disproportionately large in a subgroup of children with strictly defined autism. The findings were generally similar for boys and girls. Children with DD had smaller amygdalas (Neurology 2002;59:184–92).

Consistent with the findings of other studies, larger-than-average brains in the University of Washington autism sample leveled off in size over time, Dr. Friedman said. Some researchers have suggested that this early increase might be caused by a large number of neurons densely packed into the cortex.

To test this hypothesis, he and his associates evaluated regional brain chemistry in the same 45 children with autism and PDD-NOS, as well as 15 children with DD (the original 14 plus 1 more), and 13 of the original children in the TD group.

They used dual-proton echoplanar spectroscopic imaging to measure brain metabolite concentrations. They also measured each metabolite's relaxation time—the approximate time it takes a chemical system to return to its original state after being perturbed by an outside force, such as a change in temperature, pressure, or—in the case of magnetic resonance—radio waves. In this study, the relative measures of transverse relaxation (T2r) were calculated from the paired echoes to provide a picture of the metabolic activity within the subjects' gray matter.

Compared with the TD children, those with autism and PDD-NOS had T2r values of myoinositol, N-acetylaspartate, and creatine that were 13%, 10%, and 8% lower, respectively. These significant differences suggest there is a lower concentration of these metabolites in the gray matter. However, compared with those of the DD subjects, their T2r values for choline and creatine were 10% and 9% higher, respectively (Neurology 2003;60:100–7).

These data contradict the idea that people with autism experience dense neuronal packing early in the life, Dr. Friedman said. They may support a theory advanced by Manuel F. Casanova, M.D., of the University of Louisville (Ky.), that cortical minicolumns, self-contained organizational neuronal units found throughout the brain, are more numerous but smaller and less organized in these patients.

IRVINE, CALIF. — Children with autism and pervasive developmental disorder show abnormalities in brain structure and chemistry early in their life, Seth Friedman, Ph.D., said at the annual conference of the EEG and Clinical Neuroscience Society.

Brain-volume increases in autism are likely not present at birth but begin to develop in infancy, grow most marked by 3–4 years of age, and level off somewhat by age 6–7 years, a theory championed by Eric Courchesne, Ph.D., of the University of California, San Diego. These changes may reflect deficits in cortical volume and organization relative to that seen in children who are developing more typically, said Dr. Friedman, of the University of Washington, Seattle.

With his colleagues, Dr. Friedman compared magnetic resonance images from 45 children with autism or pervasive developmental disorder not otherwise specified (PDD-NOS) and from 14 children with other types of developmental delays (DD) with images from 26 typically developing (TD) children. All subjects were 3–4 years old.

The children in the autistic and PDD-NOS groups had significantly larger cerebral volumes than the other two groups. Their cerebellar, amygdala, and hippocampal volumes were also larger but were proportionate to the overall increase in cerebral size. However, the amygdala was disproportionately large in a subgroup of children with strictly defined autism. The findings were generally similar for boys and girls. Children with DD had smaller amygdalas (Neurology 2002;59:184–92).

Consistent with the findings of other studies, larger-than-average brains in the University of Washington autism sample leveled off in size over time, Dr. Friedman said. Some researchers have suggested that this early increase might be caused by a large number of neurons densely packed into the cortex.

To test this hypothesis, he and his associates evaluated regional brain chemistry in the same 45 children with autism and PDD-NOS, as well as 15 children with DD (the original 14 plus 1 more), and 13 of the original children in the TD group.

They used dual-proton echoplanar spectroscopic imaging to measure brain metabolite concentrations. They also measured each metabolite's relaxation time—the approximate time it takes a chemical system to return to its original state after being perturbed by an outside force, such as a change in temperature, pressure, or—in the case of magnetic resonance—radio waves. In this study, the relative measures of transverse relaxation (T2r) were calculated from the paired echoes to provide a picture of the metabolic activity within the subjects' gray matter.

Compared with the TD children, those with autism and PDD-NOS had T2r values of myoinositol, N-acetylaspartate, and creatine that were 13%, 10%, and 8% lower, respectively. These significant differences suggest there is a lower concentration of these metabolites in the gray matter. However, compared with those of the DD subjects, their T2r values for choline and creatine were 10% and 9% higher, respectively (Neurology 2003;60:100–7).

These data contradict the idea that people with autism experience dense neuronal packing early in the life, Dr. Friedman said. They may support a theory advanced by Manuel F. Casanova, M.D., of the University of Louisville (Ky.), that cortical minicolumns, self-contained organizational neuronal units found throughout the brain, are more numerous but smaller and less organized in these patients.

IRVINE, CALIF. — Children with autism and pervasive developmental disorder show abnormalities in brain structure and chemistry early in their life, Seth Friedman, Ph.D., said at the annual conference of the EEG and Clinical Neuroscience Society.

Brain-volume increases in autism are likely not present at birth but begin to develop in infancy, grow most marked by 3–4 years of age, and level off somewhat by age 6–7 years, a theory championed by Eric Courchesne, Ph.D., of the University of California, San Diego. These changes may reflect deficits in cortical volume and organization relative to that seen in children who are developing more typically, said Dr. Friedman, of the University of Washington, Seattle.

With his colleagues, Dr. Friedman compared magnetic resonance images from 45 children with autism or pervasive developmental disorder not otherwise specified (PDD-NOS) and from 14 children with other types of developmental delays (DD) with images from 26 typically developing (TD) children. All subjects were 3–4 years old.

The children in the autistic and PDD-NOS groups had significantly larger cerebral volumes than the other two groups. Their cerebellar, amygdala, and hippocampal volumes were also larger but were proportionate to the overall increase in cerebral size. However, the amygdala was disproportionately large in a subgroup of children with strictly defined autism. The findings were generally similar for boys and girls. Children with DD had smaller amygdalas (Neurology 2002;59:184–92).

Consistent with the findings of other studies, larger-than-average brains in the University of Washington autism sample leveled off in size over time, Dr. Friedman said. Some researchers have suggested that this early increase might be caused by a large number of neurons densely packed into the cortex.

To test this hypothesis, he and his associates evaluated regional brain chemistry in the same 45 children with autism and PDD-NOS, as well as 15 children with DD (the original 14 plus 1 more), and 13 of the original children in the TD group.

They used dual-proton echoplanar spectroscopic imaging to measure brain metabolite concentrations. They also measured each metabolite's relaxation time—the approximate time it takes a chemical system to return to its original state after being perturbed by an outside force, such as a change in temperature, pressure, or—in the case of magnetic resonance—radio waves. In this study, the relative measures of transverse relaxation (T2r) were calculated from the paired echoes to provide a picture of the metabolic activity within the subjects' gray matter.

Compared with the TD children, those with autism and PDD-NOS had T2r values of myoinositol, N-acetylaspartate, and creatine that were 13%, 10%, and 8% lower, respectively. These significant differences suggest there is a lower concentration of these metabolites in the gray matter. However, compared with those of the DD subjects, their T2r values for choline and creatine were 10% and 9% higher, respectively (Neurology 2003;60:100–7).

These data contradict the idea that people with autism experience dense neuronal packing early in the life, Dr. Friedman said. They may support a theory advanced by Manuel F. Casanova, M.D., of the University of Louisville (Ky.), that cortical minicolumns, self-contained organizational neuronal units found throughout the brain, are more numerous but smaller and less organized in these patients.

NEWPORT BEACH, CALIF. — Tinea capitis is the most common dermatophytic infection of childhood, Sheila Fallon Friedlander, M.D., said at the annual meeting of the Pacific Dermatologic Association.

She answered common questions posed by primary care physicians about the condition:

▸ Which organisms are most likely to cause tinea capitis? In the United States, Trichophyton tonsurans accounts for most cases, said Dr. Friedlander, a pediatric dermatologist at the University of California, San Diego, Healthcare system. Microsporum canis is occasionally seen, and usually is transmitted from a household pet.

However, in other countries, other organisms may cause tinea capitis, which is something to keep in mind when examining a child who immigrated from abroad, has recently traveled abroad, or who was adopted from a foreign country.

▸ What is the treatment of choice? Treatment should consist of oral griseofulvin plus a topical antifungal agent. Dr. Friedlander recommends starting griseofulvin at a dose of 20 mg/kg, which is higher than the standard dose but produces the best cure rates. A lower dose is “an inappropriate treatment for tinea capitis,” she said.

Evidence is accumulating that terbinafine (Lamisil), given at 3–6 mg/kg, is as safe and effective as griseofulvin and acts within 2 weeks. Enhanced efficacy has been seen with higher dosing of terbinafine (5–8 mg/kg per day). Some studies have documented good response with itraconazole (Sporanox) and fluconazole (Diflucan).

▸ How long should treatment last? In her practice, Dr. Friedlander usually treats for 8 weeks. Many experts recommend treating until 2 weeks after resolution of symptoms, which may require weeks to months of therapy.

▸ What do you tell parents about griseofulvin? Griseofulvin is inexpensive and has a long track record of efficacy. It is a relatively safe drug, but about 30% of patients develop side effects that include headache, gastrointestinal upset, and photosensitivity.

▸ Are laboratory tests necessary? Lab tests are needed only if the patient requires more than 8 weeks of treatment.

▸ Do you treat the entire family? Ask about other family members and treat them if they are symptomatic. T. tonsurans is commonly passed among wrestlers. Infection with M. canis should lead to questions about the family pet, as cats and dogs frequently harbor these organisms.

Some family members may insist on treatment even when they are asymptomatic. Dr. Friedlander prescribes topical therapy to reassure them.

▸ Do you prescribe prednisone for kerions? Most patients don't need prednisone. Kerions (nodular, exudative, circumscribed tumefactions covered with pustules) usually respond to antifungal therapy.

“We recommend adjunctive topical antifungal therapy, but rarely utilize the systemic therapy,” Dr. Friedlander said. If the patient doesn't improve within 2 weeks, Dr. Friedlander said she will add systemic therapy, but in most cases that isn't necessary.

NEWPORT BEACH, CALIF. — Tinea capitis is the most common dermatophytic infection of childhood, Sheila Fallon Friedlander, M.D., said at the annual meeting of the Pacific Dermatologic Association.

She answered common questions posed by primary care physicians about the condition:

▸ Which organisms are most likely to cause tinea capitis? In the United States, Trichophyton tonsurans accounts for most cases, said Dr. Friedlander, a pediatric dermatologist at the University of California, San Diego, Healthcare system. Microsporum canis is occasionally seen, and usually is transmitted from a household pet.

However, in other countries, other organisms may cause tinea capitis, which is something to keep in mind when examining a child who immigrated from abroad, has recently traveled abroad, or who was adopted from a foreign country.

▸ What is the treatment of choice? Treatment should consist of oral griseofulvin plus a topical antifungal agent. Dr. Friedlander recommends starting griseofulvin at a dose of 20 mg/kg, which is higher than the standard dose but produces the best cure rates. A lower dose is “an inappropriate treatment for tinea capitis,” she said.

Evidence is accumulating that terbinafine (Lamisil), given at 3–6 mg/kg, is as safe and effective as griseofulvin and acts within 2 weeks. Enhanced efficacy has been seen with higher dosing of terbinafine (5–8 mg/kg per day). Some studies have documented good response with itraconazole (Sporanox) and fluconazole (Diflucan).

▸ How long should treatment last? In her practice, Dr. Friedlander usually treats for 8 weeks. Many experts recommend treating until 2 weeks after resolution of symptoms, which may require weeks to months of therapy.

▸ What do you tell parents about griseofulvin? Griseofulvin is inexpensive and has a long track record of efficacy. It is a relatively safe drug, but about 30% of patients develop side effects that include headache, gastrointestinal upset, and photosensitivity.

▸ Are laboratory tests necessary? Lab tests are needed only if the patient requires more than 8 weeks of treatment.

▸ Do you treat the entire family? Ask about other family members and treat them if they are symptomatic. T. tonsurans is commonly passed among wrestlers. Infection with M. canis should lead to questions about the family pet, as cats and dogs frequently harbor these organisms.

Some family members may insist on treatment even when they are asymptomatic. Dr. Friedlander prescribes topical therapy to reassure them.

▸ Do you prescribe prednisone for kerions? Most patients don't need prednisone. Kerions (nodular, exudative, circumscribed tumefactions covered with pustules) usually respond to antifungal therapy.

“We recommend adjunctive topical antifungal therapy, but rarely utilize the systemic therapy,” Dr. Friedlander said. If the patient doesn't improve within 2 weeks, Dr. Friedlander said she will add systemic therapy, but in most cases that isn't necessary.

NEWPORT BEACH, CALIF. — Tinea capitis is the most common dermatophytic infection of childhood, Sheila Fallon Friedlander, M.D., said at the annual meeting of the Pacific Dermatologic Association.

She answered common questions posed by primary care physicians about the condition:

▸ Which organisms are most likely to cause tinea capitis? In the United States, Trichophyton tonsurans accounts for most cases, said Dr. Friedlander, a pediatric dermatologist at the University of California, San Diego, Healthcare system. Microsporum canis is occasionally seen, and usually is transmitted from a household pet.

However, in other countries, other organisms may cause tinea capitis, which is something to keep in mind when examining a child who immigrated from abroad, has recently traveled abroad, or who was adopted from a foreign country.

▸ What is the treatment of choice? Treatment should consist of oral griseofulvin plus a topical antifungal agent. Dr. Friedlander recommends starting griseofulvin at a dose of 20 mg/kg, which is higher than the standard dose but produces the best cure rates. A lower dose is “an inappropriate treatment for tinea capitis,” she said.

Evidence is accumulating that terbinafine (Lamisil), given at 3–6 mg/kg, is as safe and effective as griseofulvin and acts within 2 weeks. Enhanced efficacy has been seen with higher dosing of terbinafine (5–8 mg/kg per day). Some studies have documented good response with itraconazole (Sporanox) and fluconazole (Diflucan).

▸ How long should treatment last? In her practice, Dr. Friedlander usually treats for 8 weeks. Many experts recommend treating until 2 weeks after resolution of symptoms, which may require weeks to months of therapy.

▸ What do you tell parents about griseofulvin? Griseofulvin is inexpensive and has a long track record of efficacy. It is a relatively safe drug, but about 30% of patients develop side effects that include headache, gastrointestinal upset, and photosensitivity.

▸ Are laboratory tests necessary? Lab tests are needed only if the patient requires more than 8 weeks of treatment.

▸ Do you treat the entire family? Ask about other family members and treat them if they are symptomatic. T. tonsurans is commonly passed among wrestlers. Infection with M. canis should lead to questions about the family pet, as cats and dogs frequently harbor these organisms.

Some family members may insist on treatment even when they are asymptomatic. Dr. Friedlander prescribes topical therapy to reassure them.

▸ Do you prescribe prednisone for kerions? Most patients don't need prednisone. Kerions (nodular, exudative, circumscribed tumefactions covered with pustules) usually respond to antifungal therapy.

“We recommend adjunctive topical antifungal therapy, but rarely utilize the systemic therapy,” Dr. Friedlander said. If the patient doesn't improve within 2 weeks, Dr. Friedlander said she will add systemic therapy, but in most cases that isn't necessary.

SAN FRANCISCO — For people who are too old or ill to withstand the rigors of microvascular decompression, the gamma knife is a “reasonable treatment option” for recalcitrant trigeminal neuralgia, Jason Sheehan, M.D., said at the annual meeting of the Congress of Neurological Surgeons.

Microvascular decompression is the procedure with the best track record for relieving pain due to trigeminal neuralgia (TN). However, the surgery risks rare but serious complications, including brain stem infarction, cerebellar edema and hematoma, and hydrocephalus. Further, recovery often requires a stay in intensive care.

Of 136 patients, median age 68 years, who underwent radiosurgery with the gamma knife at the University of Virginia, Charlottesville, 70% reported a significant diminution of pain up to 3 years later, said Dr. Sheehan of the university. Patients included 122 with typical trigeminal neuralgia, 3 whose TN took an atypical form, 4 with facial pain associated with multiple sclerosis, and 7 whose TN was associated with a cavernous sinus tumor. A median 72 months elapsed from diagnosis to the gamma knife procedure.

One year after surgery, 90% of the patients reported significant pain relief, and 47% had no pain. At 2 years, those numbers had dropped to 77% and 45%, respectively, and at 3 years, to 70% and 34%, respectively. These findings are comparable with those of studies by different investigators, who reported pain-free outcomes of 40%-50% and an overall 70% incidence of pain relief within the first few years after surgery, Dr. Sheehan said.

SAN FRANCISCO — For people who are too old or ill to withstand the rigors of microvascular decompression, the gamma knife is a “reasonable treatment option” for recalcitrant trigeminal neuralgia, Jason Sheehan, M.D., said at the annual meeting of the Congress of Neurological Surgeons.

Microvascular decompression is the procedure with the best track record for relieving pain due to trigeminal neuralgia (TN). However, the surgery risks rare but serious complications, including brain stem infarction, cerebellar edema and hematoma, and hydrocephalus. Further, recovery often requires a stay in intensive care.

Of 136 patients, median age 68 years, who underwent radiosurgery with the gamma knife at the University of Virginia, Charlottesville, 70% reported a significant diminution of pain up to 3 years later, said Dr. Sheehan of the university. Patients included 122 with typical trigeminal neuralgia, 3 whose TN took an atypical form, 4 with facial pain associated with multiple sclerosis, and 7 whose TN was associated with a cavernous sinus tumor. A median 72 months elapsed from diagnosis to the gamma knife procedure.

One year after surgery, 90% of the patients reported significant pain relief, and 47% had no pain. At 2 years, those numbers had dropped to 77% and 45%, respectively, and at 3 years, to 70% and 34%, respectively. These findings are comparable with those of studies by different investigators, who reported pain-free outcomes of 40%-50% and an overall 70% incidence of pain relief within the first few years after surgery, Dr. Sheehan said.

SAN FRANCISCO — For people who are too old or ill to withstand the rigors of microvascular decompression, the gamma knife is a “reasonable treatment option” for recalcitrant trigeminal neuralgia, Jason Sheehan, M.D., said at the annual meeting of the Congress of Neurological Surgeons.

Microvascular decompression is the procedure with the best track record for relieving pain due to trigeminal neuralgia (TN). However, the surgery risks rare but serious complications, including brain stem infarction, cerebellar edema and hematoma, and hydrocephalus. Further, recovery often requires a stay in intensive care.

Of 136 patients, median age 68 years, who underwent radiosurgery with the gamma knife at the University of Virginia, Charlottesville, 70% reported a significant diminution of pain up to 3 years later, said Dr. Sheehan of the university. Patients included 122 with typical trigeminal neuralgia, 3 whose TN took an atypical form, 4 with facial pain associated with multiple sclerosis, and 7 whose TN was associated with a cavernous sinus tumor. A median 72 months elapsed from diagnosis to the gamma knife procedure.

One year after surgery, 90% of the patients reported significant pain relief, and 47% had no pain. At 2 years, those numbers had dropped to 77% and 45%, respectively, and at 3 years, to 70% and 34%, respectively. These findings are comparable with those of studies by different investigators, who reported pain-free outcomes of 40%-50% and an overall 70% incidence of pain relief within the first few years after surgery, Dr. Sheehan said.

IRVINE, CALIF. – Neuroimaging is offering a window into the brain structure abnormalities that underlie the unique mental and behavioral features of some rare genetic disorders, Allan Reiss, M.D., said at the annual conference of the EEG and Clinical Neuroscience Society.

In some cases, these studies may allow researchers to match specific genes with certain neurologic functions, Dr. Reiss said.

He described some of the studies he and his colleagues at Stanford (Calif.) University have conducted on individuals with Turner's and Williams syndromes.

The clinical features of Turner's syndrome (the loss of an X chromosome), which affects 1 of every 2,500 live female births, include short stature, delayed or absent puberty, and a high risk of diabetes and osteoporosis.

Affected girls usually have an IQ that is normal but may be 5–8 points lower than that of a same-sex sibling. They exhibit problems with basic emotional processing beyond what might be expected for their IQ, Dr. Reiss said. Their verbal development is normal, but they have marked deficits in visual-spatial processing.

Functional MRI studies in his lab have shown that parietal and occipital cortical volume is smaller in patients with Turner's syndrome than in controls, which could explain the visual-spatial weaknesses. Significant volume losses in the inferior parietal lobule and, in some patients, the postcentral gyrus, account for most of the parietal deficits in these patients. The hippocampus also displays mild losses of volume.

In a series of functional MRI studies comparing brain activation in 13 patients with Turner's syndrome to that of 13 normal controls, Dr. Reiss and his colleagues found that both groups activated the parietal-occipital and frontal cortices in response to a visual orientation task, but the activation was significantly less among subjects with Turner's syndrome. When confronted with a more difficult task, the controls recruited executive frontal areas, but the patients showed no such recruitment. The investigators concluded that problems in activating and deactivating neurons in the relevant brain regions may underlie the visual-spatial deficits that characterize this condition (Cereb. Cortex 2004;14:174–80).

Dr. Reiss and his associates evaluated a pair of monozygotic twins, one of whom had Turner's syndrome and the other who developed normally. Both girls had a verbal IQ in the mid-140s. However, the unaffected twin had a performance IQ of 139; her sister's was 121.

Imaging studies showed that portions of the parietal lobe and the frontal and prefrontal gyri were smaller in the affected than the nonaffected twin, yet the twin with Turner's syndrome performed as well as her sister on visual-spatial tests. She accomplished this through significantly greater activation of her parietal lobe, Dr. Reiss said.

All in all, the evidence to date suggests that structural and functional abnormalities of the parietal-occipital cortex underlie the nonverbal deficits that characterize Turner's syndrome, he said. The twin study sheds a glimmer of light on possible compensatory strategies some patients may use to overcome those deficits and raises the possibility that those strategies could be taught to other patients as well.

Boys as well as girls may have Williams syndrome (WS), which is caused by the deletion of several genes from the q11.23 region of chromosome 7. Conventional estimates place its incidence at 1 in every 20,000 live births, but the actual occurrence is probably closer to 1 in 8,000.

In one study, Dr. Reiss and his associates used volumetric analysis and voxel-based morphometry to compare the brain anatomy of 43 patients with WS to that of 40 healthy age- and sex-matched controls. The children with WS had reduced gray matter volume in the thalamus and occipital lobe and reduced gray matter density in the subcortical and cortical regions comprising the visual-spatial system. Their brains were about 13% smaller than those of the controls, with reduced occipital volume accounting for most of that difference.

IRVINE, CALIF. – Neuroimaging is offering a window into the brain structure abnormalities that underlie the unique mental and behavioral features of some rare genetic disorders, Allan Reiss, M.D., said at the annual conference of the EEG and Clinical Neuroscience Society.

In some cases, these studies may allow researchers to match specific genes with certain neurologic functions, Dr. Reiss said.

He described some of the studies he and his colleagues at Stanford (Calif.) University have conducted on individuals with Turner's and Williams syndromes.

The clinical features of Turner's syndrome (the loss of an X chromosome), which affects 1 of every 2,500 live female births, include short stature, delayed or absent puberty, and a high risk of diabetes and osteoporosis.

Affected girls usually have an IQ that is normal but may be 5–8 points lower than that of a same-sex sibling. They exhibit problems with basic emotional processing beyond what might be expected for their IQ, Dr. Reiss said. Their verbal development is normal, but they have marked deficits in visual-spatial processing.

Functional MRI studies in his lab have shown that parietal and occipital cortical volume is smaller in patients with Turner's syndrome than in controls, which could explain the visual-spatial weaknesses. Significant volume losses in the inferior parietal lobule and, in some patients, the postcentral gyrus, account for most of the parietal deficits in these patients. The hippocampus also displays mild losses of volume.

In a series of functional MRI studies comparing brain activation in 13 patients with Turner's syndrome to that of 13 normal controls, Dr. Reiss and his colleagues found that both groups activated the parietal-occipital and frontal cortices in response to a visual orientation task, but the activation was significantly less among subjects with Turner's syndrome. When confronted with a more difficult task, the controls recruited executive frontal areas, but the patients showed no such recruitment. The investigators concluded that problems in activating and deactivating neurons in the relevant brain regions may underlie the visual-spatial deficits that characterize this condition (Cereb. Cortex 2004;14:174–80).

Dr. Reiss and his associates evaluated a pair of monozygotic twins, one of whom had Turner's syndrome and the other who developed normally. Both girls had a verbal IQ in the mid-140s. However, the unaffected twin had a performance IQ of 139; her sister's was 121.

Imaging studies showed that portions of the parietal lobe and the frontal and prefrontal gyri were smaller in the affected than the nonaffected twin, yet the twin with Turner's syndrome performed as well as her sister on visual-spatial tests. She accomplished this through significantly greater activation of her parietal lobe, Dr. Reiss said.

All in all, the evidence to date suggests that structural and functional abnormalities of the parietal-occipital cortex underlie the nonverbal deficits that characterize Turner's syndrome, he said. The twin study sheds a glimmer of light on possible compensatory strategies some patients may use to overcome those deficits and raises the possibility that those strategies could be taught to other patients as well.

Boys as well as girls may have Williams syndrome (WS), which is caused by the deletion of several genes from the q11.23 region of chromosome 7. Conventional estimates place its incidence at 1 in every 20,000 live births, but the actual occurrence is probably closer to 1 in 8,000.

In one study, Dr. Reiss and his associates used volumetric analysis and voxel-based morphometry to compare the brain anatomy of 43 patients with WS to that of 40 healthy age- and sex-matched controls. The children with WS had reduced gray matter volume in the thalamus and occipital lobe and reduced gray matter density in the subcortical and cortical regions comprising the visual-spatial system. Their brains were about 13% smaller than those of the controls, with reduced occipital volume accounting for most of that difference.

IRVINE, CALIF. – Neuroimaging is offering a window into the brain structure abnormalities that underlie the unique mental and behavioral features of some rare genetic disorders, Allan Reiss, M.D., said at the annual conference of the EEG and Clinical Neuroscience Society.

In some cases, these studies may allow researchers to match specific genes with certain neurologic functions, Dr. Reiss said.

He described some of the studies he and his colleagues at Stanford (Calif.) University have conducted on individuals with Turner's and Williams syndromes.

The clinical features of Turner's syndrome (the loss of an X chromosome), which affects 1 of every 2,500 live female births, include short stature, delayed or absent puberty, and a high risk of diabetes and osteoporosis.

Affected girls usually have an IQ that is normal but may be 5–8 points lower than that of a same-sex sibling. They exhibit problems with basic emotional processing beyond what might be expected for their IQ, Dr. Reiss said. Their verbal development is normal, but they have marked deficits in visual-spatial processing.

Functional MRI studies in his lab have shown that parietal and occipital cortical volume is smaller in patients with Turner's syndrome than in controls, which could explain the visual-spatial weaknesses. Significant volume losses in the inferior parietal lobule and, in some patients, the postcentral gyrus, account for most of the parietal deficits in these patients. The hippocampus also displays mild losses of volume.

In a series of functional MRI studies comparing brain activation in 13 patients with Turner's syndrome to that of 13 normal controls, Dr. Reiss and his colleagues found that both groups activated the parietal-occipital and frontal cortices in response to a visual orientation task, but the activation was significantly less among subjects with Turner's syndrome. When confronted with a more difficult task, the controls recruited executive frontal areas, but the patients showed no such recruitment. The investigators concluded that problems in activating and deactivating neurons in the relevant brain regions may underlie the visual-spatial deficits that characterize this condition (Cereb. Cortex 2004;14:174–80).

Dr. Reiss and his associates evaluated a pair of monozygotic twins, one of whom had Turner's syndrome and the other who developed normally. Both girls had a verbal IQ in the mid-140s. However, the unaffected twin had a performance IQ of 139; her sister's was 121.

Imaging studies showed that portions of the parietal lobe and the frontal and prefrontal gyri were smaller in the affected than the nonaffected twin, yet the twin with Turner's syndrome performed as well as her sister on visual-spatial tests. She accomplished this through significantly greater activation of her parietal lobe, Dr. Reiss said.

All in all, the evidence to date suggests that structural and functional abnormalities of the parietal-occipital cortex underlie the nonverbal deficits that characterize Turner's syndrome, he said. The twin study sheds a glimmer of light on possible compensatory strategies some patients may use to overcome those deficits and raises the possibility that those strategies could be taught to other patients as well.

Boys as well as girls may have Williams syndrome (WS), which is caused by the deletion of several genes from the q11.23 region of chromosome 7. Conventional estimates place its incidence at 1 in every 20,000 live births, but the actual occurrence is probably closer to 1 in 8,000.

In one study, Dr. Reiss and his associates used volumetric analysis and voxel-based morphometry to compare the brain anatomy of 43 patients with WS to that of 40 healthy age- and sex-matched controls. The children with WS had reduced gray matter volume in the thalamus and occipital lobe and reduced gray matter density in the subcortical and cortical regions comprising the visual-spatial system. Their brains were about 13% smaller than those of the controls, with reduced occipital volume accounting for most of that difference.