Trends of back pain in eastern Finland, 1972-1992, in relation to socioeconomic status and behavioral risk factors

We report a 74-year-old woman with parkinsonism and dementia, who died 4 years after the onset of the disease. She was well until 70 years of the age (1993) when she noted slowness in the movement in her left hand. She also developed gait disturbance and the similar symptoms spread to the right upper and lower extremities. Two years after the onset, she had difficulty in walk, and was admitted to our hospital on March 9, 1995. Her daughter had the onset of hand tremor at 50 years of the age and gait disturbance at 52. Her gait improved after levodopa treatment, but her MRI revealed a liner T2-high signal lesion along the outer surface of each putamen. On admission, the patient was alert but slighted demented. Higher cerebral functions were normal. She had a masked face and small voice. Her gait was of small step without arm swing. Retropulsion was present. Rigidity was noted in the neck but not in the limbs. She was bradykinetic but tremor was absent. She was treated with levodopa/carbidopa, dops, and bromocriptine with considerable improvement and was discharged on March 30, 1995. On January 19, 1996, she developed fever and hallucination; she became more akinetic and admitted again. She showed marked dementia and stage IV parkinsonism. She was treated by supportive measures with improvement in the general condition, but she was found to have a gastric cancer for which a subtotal gastrectomy was performed on March 11, 1996. Post-operative course was uneventful, but her parkinsonism progressed to stage V. She was transferred to another hospital on May 13, 1996. In July 21, 1996, she developed dyspnea and fever and was admitted to our hospital again. She was somnolent. Rigidity was moderate to marked and she was unable to stand or walk. By supportive cares, her general condition improved and was discharged to home on November 4, 1996. She developed fever on June 13, 1997 and admitted to our service again. Her BP was 150/90 mmHg. She was alert but markedly demented. Laboratory examination revealed increases in liver enzymes (GOT 75 IU/l, GPT 101 IU/l) and renal dysfunction (BUN 68 mg/dl, creatinine 3.27 mg/dl). Subsequent hospital course was complicated by renal failure and thrombocytopenia (33,000/ml). She expired on July 1, 1997. The patient was discussed in a neurologic CPC, and a chief discussant arrived at the conclusion that the patient had diffuse Lewy body disease and her daughter striatonigral degeneration. Some participants thought both the patient and her daughter had diffuse Lewy body disease. Post-mortem examination revealed marked degeneration of the substania nigra and the locus coeruleus. The medial part of the nigra also showed marked cell loss. Lewy bodies were found in the remaining nigral and coeruleus neurons. Cortical Lewy bodies were very few and the striatum was intact. Pathologic diagnosis was Parkinson's disease. Dementia was in part attributed to the marked degeneration of the medial part of the substantia nigra.     

(Neurological CPC.55). A 60-year-old woman with progressive cerebellar ataxia, myoclonus, and dementia

We report a 60-year-old woman with progressive ataxia, myoclonus, choreoathetosis, and dementia. She was well until 27 years of the age when she noted an onset of gait disturbance and speech disturbance. She noted abnormal involuntary movements in her four limbs at 42 years of the age. Her symptoms had progressively become worse and she fell down frequently by her 52 years of the age. In addition, her family members noted gradual decline in her intelligence. She was admitted to our hospital in February of 1993 when she was 57-year-old. On admission, she showed dementia, scanning speech, ataxic gait, limb ataxia, action myoclonus, and choreic movements which involved her four limbs. Deep tendon reflexes were slightly exaggerated in the lower limbs; no Babinski sign was noted. Sensation was intact. Laboratory findings were unremarkable. Cerebral MRI revealed atrophy of the cerebellar cortex, superior cerebellar peduncle, brain stem, and the cerebral cortex; the third ventricle and the lateral ventricles were dilated; furthermore, T2-high signal lesions were seen in the cerebral white matter and in the pontine base. Her clinical course was one of the progressive deterioration of her ataxia, involuntary movements, and dementia. She expired on April 24, 1996 when she was 60-year-old. She was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had dentatorubral-pallidoluysian atrophy. A minor opinion was that she might have had myoclonus epilepsy with ragged-red fibers. Postmortem examination revealed atrophy, gliosis, and neuronal loss in the external segment of the globus pallidus, subthalamic nucleus, red nucleus, and in the dentate nucleus. In addition, the gracil and cuneiform nuclei showed neuronal loss and spheroid formation; the spinocerebellar tracts were retained. The substantia nigra and the locus coeruleus were intact. No ragged-red fibers were seen in the muscle biopsy specimen taken in February, 1993. The neuropathologic findings were consistent with the diagnosis of dentatorubral-pallidoluysian atrophy.     

The influence of recombinant human tumor necrosis factor alpha and its muteins used alone or in combination with 2-chlorodeoxyadenosine on normal and leukemic hematopoiesis in vitro

We report an 80-year-old woman with progressive muscular atrophy predominantly involving her right lower extremity. She was well until 1992 (75 years of age) when she noted an onset of weakness in her right leg which had got progressively worse. She was admitted to our service in July 1994. On admission, general physical examination was unremarkable. She was alert and well oriented without dementia. Higher cerebral functions were normal. Cranial nerves also appeared intact. She dragged her right leg in walking. Mild to moderate weakness (2/5 to 4/5) was noted in muscles in her right lower extremity more in the distal part. Deep tendon reflexes were within normal limits, and the plantar response was flexor bilaterally. Sensation was intact. Laboratory examinations were also unremarkable except for slight increase in CK which was 470 IU/l. CSF was also normal. EMG revealed neurogenic changes in the lower extremities. She was admitted to Aoki Hospital on October 21, 1994, by that time, her weakness in the right lower extremity had gotten worse in that the muscle strength of the right extensor hallucis longus was 0 and tibialis anterior 2; muscle atrophy was also prominent in her right leg; the right ankle jerk could not be elicited. In the subsequent course, weakness and atrophy appeared in her left lower extremity, however, upper extremities and cranial nerves had never been affected. Babinski sign was always negative. In February 1996, she developed delusional ideation of self persecution, and showed difficulty in communication with medical staffs. She developed fever of 38.7 degrees C on June 13, 1996 expired on the next day. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had a form of spinal muscular atrophy. Opinions were divided between ALS and spinal muscular atrophy. Post-mortem examination revealed marked loss of anterior horn neurons in the lumbar area with astrogliosis. Bunina bodies were seen in some of the remaining neurons. No myelin pallor was noted in the pyramidal tracts, however, atrophy and loss of Betz cells were noted in the motor cortex. Other cortical areas were unremarkable. The neuropathologist arrived at the conclusion that the patient had ALS. This patient was unique in that she had asymmetric atrophy and weakness limited to the lower extremities. This is quite unusual as ALS of four years duration. In addition, the patient developed some mental change which was thought to represent dementia by some participants. But no clear morphologic changes were seen to account for her mental change.     

A 64-year-old woman with progressive gait disturbance and dementia for one year

We report a 64-year-old Japanese woman who died one year after the onset of progressive gait disturbance and dementia. She noted a difficulty in holding a glass and hand tremor in June of 1996 when she was 63 years old. In July of 1996, she tended to lean toward left when she walked. She also noted truncal titubation. In November of 1996, she started to have visual hallucination and delusion in which she said "I see something is flying on the wall.", "Somebody has come into my room", and things like that. She was admitted to our service on November 22, 1996. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed disturbance in recent memory. Hasegawa's dementia rating scale was 22/30. She showed vivid visual hallucination with colors in which she saw faces of dwarfs and angels, a space ship, and others. Higher cerebral functions were normal. She showed left oculomotor palsy which was a sequel of an aneurysm and subarachnoid hemorrhage nine years before. Otherwise cranial nerves were unremarkable. She showed ataxic gait, limb ataxia, truncal titubation, and postural hand tremor. She had no weakness and no muscle atrophy. Deep tendon reflexes were within normal limits. Plantar response was flexor. Sensation was intact. Laboratory examination was also unremarkable. Complete survey for occult malignancy was negative. CSF was under a normal pressure and cell count was 1/microliter, total protein 27 mg/dl, and sugar 68 mg/dl. Cranial CT scan was unremarkable. MRI was not obtained because of the presence of an aneurysm clip in the left internal carotid-posterior communication artery junction. She showed progressive deterioration in her mental function. By January 1997, she became unable to stand or walk with marked dementia. Repeated CSF exams and cranial CT scans were unremarkable. She suffered from several episodes of aspiration pneumonia. A trial of three days methylprednisolone pulse therapy was given starting on March 7, 1997, which was of no effect on her neurologic status. On March 28, 1997, she was intubated because of acute respiratory distress syndrome. In April 2, her body temperature rose to 38 degrees C. On April 9, 1997, her blood pressure dropped and resuscitation was unsuccessful. She was pronounced dead on the same day. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had primary leptomeningeal lymphoma. Other possibilities entertained among the audience included brain stem encephalitis of unknown type, carcinomatous cerebellar degeneration plus limbic encephalitis, Creutzfeldt-Jakob disease, thalamic degeneration, and progressive multifocal leukoencephalopathy. Post-mortem examination revealed thickening and clouding of the leptomeninges; Gram-positive diplococci were found in the leptomeninges. This meningitis appeared to have been an complication in the terminal stage of her illness. Microscopic examination revealed astrocytosis in the midbrain tegmentum. Cerebral cortices showed only mild astrtocytosis. No cerebellar atrophy was seen and Purkinje cells were retained which excluded paraneoplastic cerebellar degeneration. Neuropathologic diagnosis was bacterial meningitis, however, the presence of brain stem encephalitis prior to the onset of bacterial meningitis could not be excluded. It is interesting to note that the diagnosis of the primary neurologic disease of this patient was not easy even after autopsy. As autopsy permission was obtained only for the brain, it was not clear whether or not this patient had an occult malignancy somewhere in her body, however, there was no evidence to indicate paraneoplastic degeneration of the central nervous system. As the patient did not have meningeal signs until one month before her death, it is difficult to ascribe her entire neurologic problems to her meningitis. Finally, her visual hallucination was vivid and colorful; we thought this might have been     

A case of Klippel-Trenaunay-Weber syndrome--special reference to myelopathy

A 49-year-old woman with Klippel-Trenaunay-Weber syndrome (KTW) is reported. She had characteristic features of KTW; cutaneous angiomas on her back, left knee and both plantae, varicosities on both legs, and hypertrophy of the left leg. In addition she had rare complications of KTW; asymmetric skull bone, hemicranial hypertrophy, kyphosoliosis, idiopathic hypoparathyroidism, and abnormal length of the dactyl. Her hemicranial hypertrophy was examined by CT scan, MRI and angiography. Her right hemicranial volume was enlarged and her left lateral ventricle was enlarged. The T2-weighted MRI imaging demonstrated high signal intensity beside the right lateral ventricle and in the right basal ganglia. Cerebrovascular anomalies were not revealed. She also had neurological manifestations of KTW that are rarely seen in adult cases; mental retardation, and myelopathy. The anti-HTLV-I antibodies in serum and cerebrospinal fluid were positive, so it was thought for her to have HTLV-I associated myelopathy (HAM). She was treated with peroral prednisolone and alpha-interferon (intramuscular), which improved her ability to walk. It is known that kyphosis sometimes makes the disorder of spinal cord. Although KTW is known to be associated with the spinal arteriovenous malformation, several examinations did not reveal the spinal vascular anomalies in this case. So we think the myelopathy of this case was caused mainly by the kyphoscoliosis and HAM.     

Moyamoya disease associated with pulmonary sarcoidosis--case report

A 61-year-old female presented with a unique case of moyamoya disease associated with pulmonary sarcoidosis. She was admitted for sudden onset of left temporalgia with episode of numbness on face, tongue, and upper extremity on the right side. The next morning, she had symptoms of Gerstmann syndrome and her ability to speak was disturbed. Her medical history included radical resection of lung cancer on the right side. She had no symptoms of pulmonary sarcoidosis. Neuroimaging showed an infarction in the left occipital lobe. Angiography showed occlusions of the bilateral internal carotid arteries at the supraclinoid portions. Subsequently, a left superficial temporal artery-middle cerebral artery anastomosis with encephalo-myo-synangiosis was performed. Ninety-three days after admission, she suddenly developed dyspnea which resulted in death 3 hours later. Autopsy findings showed typical epithelioid granulomas of sarcoid type in the lymph nodes of the peribronchus, lung, and liver. Thrombotic emboli were found in the bilateral pulmonary arteries, and marked fibrous intimal thickening in the bilateral internal carotid arteries. Immunological reaction with inflammatory events may cause pathological changes in patients with moyamoya disease or sarcoidosis. The co-incidence in this case suggests that some common inflammatory events may be involved in the pathogenesis of these diseases.     

Thalamic thought disorder: on being "a bit addled"

Humans can generate and maintain relatively coherent trains of thought in natural discourse. The neural mediation of this ability and the phenomenology of its breakdown are not well understood. We report a case of a woman with paramedian thalamic strokes involving the mammillothalamic tract, intralaminar nuclei, parts of the dorsomedial and ventral lateral nuclei bilaterally. She presented with a dense amnesia and confusion typical of the syndrome of bilateral paramedian thalamic infarcts. Her Tc-99m HMPAO brain SPECT scan showed decreased thalamic and basal ganglia blood flow. General diminution of cerebral blood flow and areas of further diminution in the right frontal, left temporal and left temporoparietal regions were also observed. Although her amnesia was characteristic of diencephalic amnesia, her most striking clinical feature was a bizarre, disconnected and at times incoherent speech output. Analysis of her speech revealed relatively preserved lexical and morpho-syntactic linguistic production. By contrast, analysis of the macrostructure of her discourse revealed frequent unpredictable topic shifts that were completely unconstrained by contextual factors. Many of her shifts were intrusions from previous topics. We interpret her severely disordered speech output as representing the surface manifestations of a thought disorder (rather than as a language disorder per se) characterized by an inability to maintain and appropriately shift themes that normally guide discourse. Median and intralaminar thalamic nuclei appear to be critical for the neurophysiologic regulation of thalamocortical and striatocortical circuits, which in turn may be critical for the functional regulation of contextually appropriate transitions of thought.     

Human papillomavirus-specific serologic response in vulvar neoplasia

We describe a case of positional dyspnea due to compression of the tracheobronchial tree by an extensive thoracic aneurysm. In a 77-year-old woman with long-standing systemic hypertension, intermittent anterior chest pain gradually developed over several years. She had no history of asthma or thoracic trauma. She was admitted to our hospital because of sudden, severe shortness of breath. The breathlessness was markedly worse when she lay on her back or on her right side. On physical examination, she was in acute respiratory distress with cyanosis, severe hypertension (180/110 mmHg), tachycardia, and inspiratory stridor. A chest X-ray film showed loss of volume and nearly complete radiopacity of the left hemithorax. Arterial blood gas analysis revealed an arterial oxygen partial pressure of 54.8 mmHg, a carbon dioxide partial pressure of 39.8 mmHg, and an oxygen saturation of 84.5 percent on room air. Computed tomographic examination of the thorax showed dilation of the aortic arch and descending aorta, and marked compression of the trachea and the left main bronchus. Examination with a fiberoptic bronchoscope revealed extrinsic compression of the trachea just proximal to the carina. The patient's symptoms stabilized. However, she did not undergo surgery because of her age and because of the size of the aneurysm. She died due to rupture of the aneurysm.     

Subarachnoid hemorrhage and pontine hemorrhage followed by an embolization procedure of left occipital giant arteriovenous malformation: a case report

A 42-year-old woman suddenly developed headache and nausea on July 26, 1991, and the computed tomography (CT) scan showed a moderate-sized hematoma in the left occipital lobe. After one month's conservative treatment, she had recovered to a neurologically intact state. Cerebral angiography demonstrated a giant arteriovenous malformation fed by enlarged branches of the left posterior cerebral artery as well as small branches arising from the middle cerebral artery, anterior cerebral artery and the meningeal branches of the middle meningeal artery and the occipital artery. Preoperative embolization was planned on February 24, 1992. During an attempt at catheterization of the basilar artery and the left posterior cerebral artery with a balloon catheter and a Tracker-18 catheter, the patient complained of an intensification of her headache, nausea and vomiting. So the embolization procedure was stopped. The CT scan taken immediately at that time showed a severe subarachnoid hemorrhage (SAH). She became comatose about 40 minutes later. CT scan taken next day revealed also a complication of the pontine hemorrhage. Neurologically, she had gradually recovered and could communicate with some simple words 3 months after SAH. The total removal of the AVM was performed on May 26, 1992. Postoperative course was uneventful. She showed rapid and remarkable improvement in her neurological state suggesting that the blood flow in the surrounding brain area had been corrected. A blood deficit had no doubt been caused when blood had been stolen by the giant AVM.(ABSTRACT TRUNCATED AT 250 WORDS)     

A case of clinically diagnosed Creutzfeldt-Jakob disease with serial MRI diffusion weighted images

We reported MRI findings in a 49-year-old woman with clinically diagnosed Creutzfeldt-Jakob disease (CJD). She was admitted to our hospital because of confusion, which initially appeared 5 weeks prior and was rapidly worsened. Two weeks later, she developed myoclonic jerks in her extremities with periodic synchronous discharges on EEG. Six months later, she became mutic. Brain MRI at 3 weeks after the admission demonstrated high signal intensities in the bilateral caudate nuclei and putamina on T2 weighted images (T2WIs). Diffusion weighted images (DWIs) showed hyperintensities in the basal ganglia and in the parietal and occipital cortices. Five weeks later, the abnormal intensities in the basal ganglia were still observed on T2WIs but decreased on DWIs. Five months later, the increased signal intensities in the basal ganglia had disappeared both on T2WIs and DWIs, but new hyperintensities appeared in the insula and the temporal area on DWIs. We concluded that DWIs may be useful for the demonstrations of a lesion in the cerebral cortex and the spread of lesions.     

Virginia Staudt Sexton (1916–1997).

Presents an obituary for Virginia Staudt Sexton. Sexton was born on August 30, 1916, in New York City, where she spent her life and career. She graduated cum laude from Hunter College with a major in classics and was elected to Phi Beta Kappa. She first taught elementary school and then completed a PhD in experimental psychology at Fordham University. Her first academic appointment was at Notre Dame College of Staten Island. In 1953 she moved, as Instructor, to Hunter College in the Bronx (later renamed Herbert H. Lehman College), from which she retired in 1979 as Professor Emerita. She immediately resumed her career, however, as Distinguished Professor of Psychology at St. John's University in Jamaica, New York, a position from which she retired in 1990. Sexton was a Fellow of eight divisions of the American Psychological Association (APA) and a member of six more. She began to list history as her major field of interest in APA directories as early as 1957, and it retained its importance in her entries from then on. Sexton died in 1997. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Carolyn Wood Sherif (1922-1982).

Presents an obituary for Carolyn Wood Sherif, who lived the issues that she studied as a social psychologist, explained as a teacher, and championed as an advocate of women's issues in psychology. She conducted research in the areas of the self-system, intergroup conflict and cooperation, and social judgment, and also assumed a leadership role in psychology, both nationally and internationally. Her commitment to social psychology and her enthusiasm for sharing that commitment with others made her a remarkable leader and teacher. Dr. Sherif received the Association for Women in Psychology's Distinguished Publication Award in 1981, and the APA's award for Distinguished Contribution to Education in Psychology in 1982, and in 1982 she became the editor of the Journal of Social Issues. She died after a brief illness on July 23, 1982. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Guided tissue regeneration therapy of 203 consecutively treated intrabony defects using a bioabsorbable matrix barrier. Clinical and radiographic findings

We report a 64-year-old woman who developed nausea, headache, and consciousness disturbance. She was well until four years before the onset of her neurologic illness when (April of 1990 at her 59 years of the age) she was found to have an early cancer in her anterior wall of the lower stomach. Subtotal gastrectomy was performed and the operative result was reported as curative. Four years after the surgery (December of 1994 at her 64 years of the age), she noted suboccipital headache and nausea which had become progressively worse and she was admitted to our service on May 24, 1995. On admission, she appeared chronically ill but general physical examination was unremarkable with normal vital signs. Neurologically she was alert and not demented, and the higher cerebral functions were intact. Cranial nerves were also unremarkable. She was able to walk in tandem and on heels. No motor weakness or ataxia was noted. Deep tendon reflexes were moderately increased, however, no Babinski sign was noted. Although she had headache, no meningeal signs were seen. Slight superficial and vibratory sensory loss was noted in both feet. Routine blood work was again unremarkable except for slight increase in CEA to 8.3 ng/dl (N < 5 ng/dl). The opening pressure of lumbar CSF was 180 mm H2O and the CSF contained 39 cells/microliter, 79 mg of protein, and 10 mg/dl of glucose. Approximately half of the cells were atypical malignant cells. Plain CT was unremarkable, however, tentorial border showed enhancement after contrast infusion. FGS showed no malignant tumors in the stomach. She was treated with intravenous glycerol and whole brain radiation, however, she continued to complain of severe headache, and her sensorium started to be disturbed one month after the admission. Follow-up cranial CT scan revealed enlargement of the lateral and the third ventricles. Her consciousness progressively deteriorated and she became comatose three months after the admission. Repeated cranial CT scan showed enlargement of the ventricles, but no mass lesions were seen within the brain. She developed respiratory arrest on September 25 of the same year. She was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had a gastric cancer with meningeal seeding developing meningeal carcinomatosis. The cause of deep coma was ascribed to damage of cerebral cortical areas secondary to metastatic carcinoma cells and fibrinous materials in the surface of the brain. Postmortem examination revealed thickening and clouding of leptomeninges of the cerebral convexity. On histologic observation, patchy areas of fibrous thickening were seen in the cerebral leptomeninges; in such areas, adenocarcinomatous cells were seen scattered. The basal meninges were free of carcinoma cells, however, leptomeninges of the cerebellum and brain stem tegmentum contained scattered carcinoma cells. The lateral and the third ventricles were enlarged, however, insides of the brain were free of pathologies; the ependymal layer were intact. In the stomach no carcinoma cells were remaining. Pneumonic changes were seen in the right upper and the left lower lobes which appeared to be the direct cause of her death. No evidence of tentorial herniation was noted. The cause of her deep coma was not clearly determined, however, combination of hydrocephalus and cortical malfunction due to leptomeningeal carcinoma cell infiltration and fibrinous material accumulation appeared to have played a role.     

"With a little help from my friends I get by": self-help books and psychotherapy. Essay review

A Bosnian mental health professional told the following story: Her village had been under siege for months, and she had worked around the clock in her community using all her personal and professional resources. She was offered a few days break in Zagreb and went to the city; she welcomed the chance to be out from under fire and to rest. A bookstore was the first place she wanted to go, to browse, to expand her vision, to read about other places and peoples. In the shop, the shelves were lined with American best-selling self-help books with titles like "Getting rid of the shoulds in your life in 24 hours," "How to stop being angry and guilty in 12 steps," etc. She looked at these and felt so unreal that she fled back to her village, preferring the reality of her people and her problems.     

Norma Estelle Cutts (1892–1988).

Presents an obituary for Norma Cutts. Cutts is important to the history of school psychological services because she exemplified leadership and made lasting contributions to the field. She was among the earliest psychological examiners in her state and assumed a leadership role. Her early work fostered the growth of special classes and encouraged the establishment of the Division of Special Education and Standards in the Connecticut State Department of Education in 1921. Cutts exemplified the leadership provided by women in the development of psychological services to children. Her pursuits were atypical of women generally; she was college educated, pursued career interests rather than marriage and childrearing, and was employed in several positions often reserved for men. She remained single until age 80. Born in the year that APA was founded, at the time of her death she was among the oldest living APA members. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

When do infants need additional inspired oxygen? A review of the current literature

A previously healthy 8-month-old infant experienced a dramatic change in affect, motor patterns, and appetite after a brief (4-day) separation from her parents. She went from being a happy, interactive, and engaging child to being withdrawn, with limited vocalization, spontaneous motor activity, or interest in her environment. For the first 3 days after her parents returned home, she refused solid food and most of the formula or water she was offered. Over the following week, her appetite increased minimally. Her parents were concerned about her apathy, excessive quietness, and lack of interest in food, toys, or their own attempts to engage her in play. At the pediatrician's office, she was significantly less interactive and playful compared with previous visits. Her temperature, heart rate, and respiratory rate were normal. Although there were no objective signs of dehydration, her weight was 8 ounces less than the previous recorded weight 1 month ago. Results of the physical examination were normal, with the exception of neurological and behavioral findings. She had mild, generalized decreased tone and strength, with normal deep tendon reflexes, a sad facial appearance with sustained furrowing of the lines in her forehead, difficulty in eliciting a social smile, and limited spontaneous sounds. There was an absence of focal neurological findings, a flat open anterior fontanel, and a head circumference measurement consistent with previous recorded results. There were no cutaneous bruises, and findings of her funduscopic examination did not reveal retinal hemorrhage. Before the 4-day holiday, child care was provided almost exclusively by her mother at home. On only two previous occasions, at 4 and 6 months of age, this first child of 20-year-old high school graduate parents was cared for by a neighbor when the parents went out to a movie theater. She cried for about 10 minutes when the parents left on these occasions. Her mother stated that she felt anxious about leaving the child for several days, but she and her husband decided that they needed a break and planned the 4-day vacation. Child care was provided by the neighbor, who did not notice any unusual behavior or refusal to feed while in her care during the parents' absence.     

Ischemic strokes secondary to vitamin B12 deficiency-induced hyperhomocystinemia

A 45-year-old woman sustained two ischemic cerebral infarctions 16 years after ileal resection for Crohn's disease. Her evaluation showed an elevated random serum homocystine level, a low serum vitamin B12 level, and an increased mean corpuscular volume (MCV) without anemia. A methionine-loading test resulted in a marked increase in the homocystine levels 2, 4, and 6 hours after the load. A Schilling test demonstrated a malabsorption of vitamin B12. Vitamin B12 injections normalized her fasting homocystine level and her MCV. She has had no recurrent strokes during a year follow-up.     

Leta Stetter Hollingworth: Champion of the psychology of women and gifted children.

L. S. Hollingworth (1886–1939), one of the most neglected pioneers of educational psychology, successfully challenged the prevailing scientific doctrine of women's inferior intelligence. Later in her career she established the field of gifted education, offering the 1st course and textbook in this area. In her tenure at Teachers College, Columbia University, she contributed major textbooks on mental retardation, adolescent psychology, and specific disabilities, as well as 80 scholarly papers. As the 1st psychologist in New York City, she helped establish professional standards for the field and was one of the few academicians who promoted and provided psychological services in the schools. She used the schoolroom as a laboratory for research. Her standards for research are exemplary even in modern times. Hollingworth was a courageous early leader in educational psychology who has finally begun to receive the recognition she deserves. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Common phobias

Mrs. Brown, a 65-year-old woman, was terrified of being alone at night and suffered from nyctophobia. Her husband had been dead for several years, and her 40-year-old son lived in another state with his family. She often called him in the middle of the night in a state of panic, and he felt helpless about her situation. She lived in a senior housing community that never had any problems with crime. Nonetheless, she lived in a continual stage of anxiety.     

Progressive loss of speech output with festinating speech--a case report]

Primary progressive aphasia is a rare disorder of unknown cause. We report a patient with progressive loss of speech output, a clinical variant of PPA, characterized by festinating speech. A 60-year-old right handed woman was admitted to our hospital, because of progressive deterioration of her speech. On admission, she was alert and orientated without dementia. A severe impairment of her articulation was observed: her speech rate was so fast that her speech became almost intelligible. The orofacial apraxia and difficulty in tapping were also present. The other neurological findings were normal. Neuroradiological studies showed the left perisylvian atrophy. Festinating speech has not been previously reported in patients with PPA; patient with PPA usually show a slow speech rate with effortful expression. Since festinating speech is occasionally present in the extrapyramidal disorders, such as Parkinson's disease, progressive supranuclear palsy, or pure akinesia, it appears likely that the combined lesions of the perisylvian region and the basal ganglia are responsible for her characteristic speech disorder with festinating speech.