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Biomedical subjects

M F Mendez

Publications and source records attributed to M F Mendez.

At least 19 recordsLinked to original sources
PubMed2001

Agnosia for familiar faces and odors in a patient with right temporal lobe dysfunction.

The authors studied a 53-year-old man with progressive prosopagnosia and inability to recognize his favorite foods by smell. He could not identify pictures of familiar faces, but he could match unfamiliar faces and distinguish them from familiar ones. He could not identify familiar odors, but he could detect them and could perceive them as pleasant or familiar. Neuroimaging revealed temporal lobe changes, especially on the right. Right temporal lesions may produce face and odor agnosia by preventing perceptual familiarity units from accessing semantic associations.

Agnosia↗
PubMed2001

Generalized auditory agnosia with spared music recognition in a left-hander. Analysis of a case with a right temporal stroke.

After a right temporoparietal stroke, a left-handed man lost the ability to understand speech and environmental sounds but developed greater appreciation for music. The patient had preserved reading and writing but poor verbal comprehension. Slower speech, single syllable words, and minimal written cues greatly facilitated his verbal comprehension. On identifying environmental sounds, he made predominant acoustic errors. Although he failed to name melodies, he could match, describe, and sing them. The patient had normal hearing except for presbyacusis, right-ear dominance for phonemes, and normal discrimination of basic psychoacoustic features and rhythm. Further testing disclosed difficulty distinguishing tone sequences and discriminating two clicks and short-versus-long tones, particularly in the left ear. Together, these findings suggest impairment in a direct route for temporal analysis and auditory word forms in his right hemisphere to Wernicke's area in his left hemisphere. The findings further suggest a separate and possibly rhythm-based mechanism for music recognition.

Aged↗
PubMed2001

Visuospatial deficits with preserved reading ability in a patient with posterior cortical atrophy.

Visuospatial deficits are characteristic of posterior cortical atrophy (PCA). A 58 year old woman had progressive dressing apraxia and environmental disorientation but continued to read voraciously. Positron emission tomography revealed hypometabolism of the occipitoparietal regions bilaterally, consistent with PCA. The symptoms suggested predominant dysfunction of the dorsal ("where") stream with abnormalities in visual localization and visuospatial integration; however, the patient also had a less pronounced apperceptive object agnosia. Further analysis of her preserved reading ability was performed. Familiar irregular words were read rapidly, but nonsense words were read slowly in a letter-by-letter fashion. She had a word superiority effect for embedded words and words with obscured letters but had difficulty reading stylized script or printing in unusual fonts. These findings suggested a dissociation between reading routes. Although the patient had a phonological dyslexia, her visuospatial processing was sufficient for access to preserved visual word forms for efficient lexical reading.

Agnosia↗
PubMed2001

Emergent neuroleptic hypersensitivity as a herald of presenile dementia.

Neuroleptic hypersensitivity is characteristic of dementia with Lewy bodies (DLB) but not of other dementias. The authors report 5 patients with psychotic mood disorders and long-standing antipsychotic drug therapy. As they reached 50 to 60 years of age, they unexpectedly developed hypersensitivity to these medications, with rigidity, muteness, or the neuroleptic malignant syndrome. Nearly coincident with this reaction, they developed progressive cognitive deficits consistent with frontotemporal dementia. These patients illustrate emergent neuroleptic hypersensitivity as an early manifestation of other dementias. The predisposition to neuroleptic hypersensitivity could result from depleted nigral dopaminergic neurons suggested by "smudging" of the substantia nigra pars compacta on magnetic resonance imaging.

Alzheimer Disease↗
PubMed2000

Mania in neurologic disorders.

Neurologic disorders can produce "secondary" mania. Clinicians must distinguish secondary mania from primary, idiopathic manic-depressive illness (MBI). In addition to medical and drug-induced causes of secondary mania, neurologic causes usually develop in older patients who may lack a strong family history of MDI. Neurologic causes of mania include focal strokes in the right basotemporal or inferofrontal region, strokes or tumors in the perihypothalamic region, Huntington's disease and other movement disorders, multiple sclerosis and other white matter diseases, head trauma, infections such as neurosyphilis and Creutzfeldt-Jakob disease, and frontotemporal dementia. Patients with new-onset mania require an evaluation that includes a thorough history, a neurologic examination, neuroimaging, and other selected tests. The management of patients with neurologic mania involving correcting the underlying disorder when possible and the judicious use of drugs such as the anticonvulsant medications.

Antimanic Agents↗
PubMed2000

Pedophilia and temporal lobe disturbances.

Paraphilias may occur with brain disease, but the nature of this relationship is unclear. The authors report 2 patients with late-life homosexual pedophilia. The first met criteria for frontotemporal dementia; the second had bilateral hippocampal sclerosis. Both were professional men with recent increases in sexual behavior. In both, 18-fluorodeoxyglucose positron emission tomography revealed prominent right temporal lobe hypometabolism. These cases and the literature suggest that bilateral anterior temporal disease affecting right more than left temporal lobe can increase sexual interest. A predisposition to pedophilia may be unmasked by hypersexuality from brain disease. These observations have potential implications for all neurologically based paraphilias.

Aged↗
PubMed2000

Corticobasal ganglionic degeneration with Balint's syndrome.

Corticobasal ganglionic degeneration (CBGD) is a neurodegenerative dementia characterized by asymmetric parkinsonism, ideomotor apraxia, myoclonus, dystonia, and the alien hand syndrome. This report describes a patient with CBGD who developed Balint's syndrome with simultanagnosia, oculomotor apraxia, and optic ataxia.

Aged↗
PubMed2000

Eye movement abnormalities during reading in patients with Alzheimer disease.

OBJECTIVE: This goal of this study was to evaluate reading ability by assessing eye movements during reading among patients with Alzheimer disease (AD) compared with normal elderly controls. BACKGROUND: Reading is disturbed in patients with AD. These patients may have changes in reading ability early in the course of their disease before clinical alexia or abnormalities are apparent on standard reading tasks. METHOD: Reading competence was evaluated by recording eye movements during reading in 14 patients with mild to moderate clinically probable AD and 14 age- and education-matched controls. RESULTS: All patients with AD could recognize letters and words and could understand written material of similar difficulty. Despite successful reading comprehension among the patients with AD, their oculographs showed slowed reading and irregular eye movements. Compared with controls, the patients with AD did not differ in saccadic duration; however, they had significantly longer fixation times, more forward saccades per line of text, and more saccadic regressions. In addition, increased reading difficulty significantly correlated with a scale of dementia severity in the patients with AD. CONCLUSIONS: This pattern of eye movements corresponds to increased text difficulty and probably represents difficulty with lexical-semantic access in AD. These results suggest that disordered eye movements can signal difficulties in reading ability in AD even before complaints of reading difficulty or abnormalities on reading tests and may be a means of identifying linguistic impairment early in this disorder.

Aged↗
PubMed1999

Involuntary laughter and inappropriate hilarity.

Laughter is a particularly human behavior. Neuropsychiatrists are faced with disorders of laughter, yet the nature of this behavior and its disturbances remains obscure. The authors report an unusual patient with involuntary and unremitting laughter for 20 years and review the literature. The nature of laughter suggests that it has a unique role in human communication, particularly in the social exploration of incongruous information. The disorders of laughter suggest a neuroanatomical circuitry that includes the anterior cingulate gyrus, caudal hypothalamus, temporal-amygdala structures, and a pontomedullary center. Treatment includes the use of antidepressant and antimanic agents for disorders of laughter.

Aged↗
PubMed1999

Multiple sclerosis presenting as catatonia.

OBJECTIVE: Catatonic disorder due to general medical condition must be excluded in psychiatric patients presenting with this movement disorder. This report emphasizes the association of catatonia with multiple sclerosis. METHOD: A patient with catatonia, psychotic depression, and the subsequent diagnosis of multiple sclerosis is described and the literature reviewed. RESULTS: Mutism, immobility, cataplexy, waxy flexibility, and other aspects of catatonia occur in multiple sclerosis, usually as a consequence of a severe mood disorder and extensive cerebral demyelination. These symptoms may be the presenting manifestations of multiple sclerosis. CONCLUSIONS: A high index of suspicion for neurological disease is indicated in patients with new-onset catatonia. Neuroimaging and other studies may reveal underlying demyelination requiring specific therapy.

Adult↗