Ritsuo Hashimoto

Contribution of the Supplementary Motor Area and Anterior Cingulate Gyrus to Pathological Grasping Phenomena

To investigate the relationship between the site of brain damage and characteristics of the pathological grasping phenomena, we examined different varieties of the reaction in a consecutive series of 28 patients with unilateral hemispheric damage due to stroke. Patients with a lesion relatively confined to the supplementary motor area (n = 4) constantly exhibited a grasp reflex, mainly in the hand contralateral to the lesion, but they never showed a groping reaction. By contrast, patients with damage primarily involving the anterior cingulate gyrus (n = 3) developed the groping reaction in the hand contralateral to the lesion, but they had only a very mild grasp reflex in that hand. Patients with damage involving both the supplementary motor area and the anterior cingulate gyrus (n = 12) showed the grasp reflex and groping reaction mainly in the hand contralateral to the lesion. Patients with damage to the medial parietal lobe (n = 2), those with damage to the lateral convexity of the hemisphere (n = 6), and a patient with damage confined to the corpus callosum did not exhibit such grasping phenomena. From these observations, we conclude that the grasp reflex is closely related to a lesion of the supplementary motor area, whereas the groping reaction is bound to a lesion of the anterior cingulate gyrus.

Postencephalitic focal retrograde amnesia after bilateral anterior temporal lobe damage

Background: Marked retrograde amnesia with no or almost no anterograde amnesia is rare. Recently, a combination of ventrolateral prefrontal and temporopolar cortical lesions has been suggested as the cause of such isolated or focal retrograde amnesia. It is also assumed that when the right-sided cortical structures are damaged, autobiographical episodic memories are affected. Objective: To search for new anatomic substrates for focal retrograde amnesia. Methods: We performed extensive neuropsychological tests and obtained detailed neuroimages on a 43-year-old woman who showed a severe, persistent retrograde amnesia but only a limited anterograde amnesia after probable herpes simplex encephalitis. Results: Tests of autobiographical memory revealed that she had a memory loss extending back to her childhood for both semantics and incidents; however, the ability to recall specific episodes appeared much more severely impaired than the ability to recall factual information about her past. The patient also showed profound impairments in recalling public memories; however, her scores improved nearly to a control level on forced-choice recognition memory tasks, although the recall of memories for a decade just before her illness remained mildly impaired. MRI revealed focal pathologies in the temporal poles and the anterior parts of the inferotemporal lobes on both sides, predominantly on the left, with some extension to the anterior parts of the medial temporal lobes. There was additional damage to the left insular cortex and its surrounding structures but no evidence of frontal lobe damage on MRIs or cognitive tests. Conclusions: A profound retrograde amnesia may be produced by damage to the bilateral temporal poles and anterior inferotemporal lobes in the absence of frontal lobe pathologies, and a dense and persistent episodic old memory loss can arise even with a relatively small lesion in the right anterior temporal lobe if it is combined with extensive damage to the left.

Utilization behavior after right thalamic infarction

We report a patient who showed exaggerated responses to external cues (utilization behavior), motor impersistence, and a right-hand-predominant instinctive grasp reaction after right thalamic infarction. High-resolution computed tomography with stereotaxic lesion localization revealed almost complete destruction of the ventroanterior nucleus and intralaminar nuclei of the right thalamus; the dorsomedial nucleus was only partially involved. Single photon emission computed tomography revealed hypoperfusion in the right thalamus and over the entire right cerebral cortex with some prominence in the frontal area. From these observations, we believe that the utilization behavior in our case was caused by the disturbance in maintaining cortical tone of the right hemisphere as well as by the dysfunction of the right frontal lobe, both secondary to the damage to the right ventroanterior nucleus and intralaminar nuclei.

Amnesic confabulatory syndrome after focal basal forebrain damage

Article abstract A 73-year-old woman developed amnesic confabulatory syndrome after a right focal basal forebrain hemorrhage. The confabulation, despite persistent antegrade amnesia, gradually subsided with improvement of the frontal executive function. The lesion appeared to disrupt connections of the medial and lateral limbic circuits important for memory. Simultaneous dysfunctioning of the two circuits involving the medial temporal and frontal lobes may be necessary for the development of this syndrome.

Heading Disorientation: A New Test and a Possible Underlying Mechanism

Background/Aims: Heading disorientation (HD) is a type of pure topographical disorientation. Reported cases showing HD have been very few so far, and its underlying mechanism remains unclear. The aim of this study is to find the anatomic substrates of HD and to demonstrate a possible underlying mechanism for the symptom. Methods: We investigated 3 patients with HD by a new test, the card-placing test (CPT). Part A of the test assesses the ability of a subject to retain information on spatial locations of cards placed on the floor around the subject. Part B examines the subject’s ability to integrate information on the spatial locations of similarly arranged cards and that on changes of the body directions. Results: The patients had a lesion that commonly involved the right retrosplenial cortex and showed good record results for part A but very poor ones for part B. Conclusions: The results of the CPT suggest that HD patients cannot integrate information on the spatial locations of objects derived from an egocentric reference frame with that on changes of the body directions. The retrosplenial cortex may be the place where these different types of information necessary for navigation converge.

Selective Kana jargonagraphia following right hemispheric infarction

A strongly right-handed Japanese man showed an unusual writing disorder associated with Broca-type aphasia after suffering a right hemispheric infarction. Writing with his right hand produced a fluent output in contrast to his nonfluent speech. The patients agraphia disproportionately affected the writing of kana (Japanese syllabograms), leaving relatively intact the writing of kanji (Japanese ideograms). His kana agraphia, consisting of substitutions, intrusions, transpositions, and deletions, became apparent as the number of syllables in target words increased. Quantitative analysis of the substitutions in terms of their phonological similarity to the target revealed that most of the substitutions were phonologically dissimilar. Those errors were distributed almost identically for familiar and novel words. Moreover, the errors were observed asymmetrically across the target: more errors occurred near the end than at the beginning of a word. The kana agraphia in association with fluent writing output resulted in kana jargonagraphia. These observations suggest that our patients selective kana jargonagraphia is best explained by selective damage to the hypothesized kana graphemic buffer and by disinhibition of the motor engrams of writing behavior, both of which resulted from right hemispheric damage.

The Card Placing Test: a new test for evaluating the function of the retrosplenial and posterior cingulate cortices.

Background/Aim: We developed a test named the Card Placing Test (CPT), which is potentially useful for evaluating a function of the retrosplenial and posterior cingulate cortices (RSC/PCC). Part A of the test assesses the ability of a subject to retain information on spatial locations of cards placed on the floor around the subject. Part B examines the subjects ability to integrate information on the spatial locations of similarly arranged cards and information on changes in body direction. The aim of this study is to identify brain regions involved in the CPT performance. Subjects and Methods: Twenty-five subjects were recruited from our memory clinic. We analyzed the correlation between the CPT scores and resting state regional cerebral blood flow (rCBF) determined by single-photon emission tomography. Results: The scores for part A correlated with rCBF in the right inferior parietal lobule. The scores for part B were associated with rCBF in the RSC/PCC. Conclusions: The right inferior parietal lobule seems to play a pivotal role in performing part A of the CPT, whereas the RSC/PCC appears to be involved in accomplishing part B of the CPT.

Hepatitis C virus (HCV) reactivation during fingolimod treatment for relapsing and remitting multiple sclerosis

We here report a case involving a 38-year-old female with relapsing and remitting multiple sclerosis who developed reactivation of hepatitis C virus (HCV) during administration of fingolimod for 16 months. She had been previously treated for chronic hepatitis C with pegylated interferon and ribavirin, and kept an undetectable HCV-RNA state for more than 4 years before fingolimod starting. Although the increased risk for viral reactivation, for example of herpes zoster virus and varicella-zoster virus, during fingolimod treatment is known, this is, to our knowledge, the first case report of HCV reappearance.

Heading Disorientation after Right Posteromedial Infarction

We report the case of heading disorientation following ischemic stroke involving the right posteromedial areas. The patient was administered a new test named the Card Placing Test during which a subject was required to recreate an array of three cards, each of which was randomly placed on eight grids around the subject, before and after the subjects rotation. Qualitative analysis of his performance after rotation revealed that over half of the errors comprised transposition and rotational offset. His score on the Card Placing Test was compared with those of normal controls (n = 11). The results showed that his score on Card Placing Test after rotation was significantly lower than those of controls, whereas there was no significant difference between the case and controls in profile of error types. We infer that the heading disorientation observed in the present case was a result of a derangement of a short-term buffer that integrated information on spatial locations of objects with changes in body directions.

Anti-NMDA receptor antibody-positive meningoencephalitis with SIADH and CNS demyelination: A case report

After a 34-year-old female developed a headache and high fever, she was diagnosed with aseptic meningitis. On admission, neurological examinations revealed cerebellar limb ataxia, horizontal gaze paretic nystagmus, and pyramidal tract signs. Laboratory tests showed hyponatremia (129 mEq/l). Five days after admission, convulsions in the upper limbs due to the severe hyponatremia (108 mEq/l) were noted. In addition, serum antidiuretic hormone levels were markedly increased to 18.5 pg/ml. Brain MRI showed multiple small inflammatory lesions in the subcortical cerebral white matter, thalamus, and around the third ventricular diencephalic regions. Pulse corticosteroid treatment promptly improved her symptoms. Although tests for serum anti-aquaporin 4, anti-myelin oligodendrocyte glycoprotein, and anti-voltage-gated potassium channel antibodies were negative, cerebrospinal fluid samples tested positive for anti-N-methyl-D-aspartate (NMDA) receptor antibodies. Oral prednisolone administration was continued, but she developed paresthesia in her upper and lower extremities and gaze-evoked nystagmus three months after the first attack. MRI showed that the previously observed high-intensity regions were decreased, but a new area of high intensity was observed in ventral regions through the lower midbrain to the pons. Because pulse corticosteroid treatment was again effective, we continued the oral prednisolone treatment. This case presented none of the characteristic symptoms of anti-NMDA receptor antibody encephalitis during the clinical course other than repeated demyelinating encephalitis and severe syndrome of inappropriate antidiuretic hormone secretion (SIADH). Additional clinical observations are needed to better understand the underlying pathology of the NMDA receptor antibodies in the cerebrospinal fluid in this case.