Visual and tactile agnosia

A patient presented with visual and tactile agnosia due to a spontaneous left occipito-temporal hematoma. Major memory and spatial orientation disorders were also noted, but language, gestures, auditory and olfactory perception, and interior visual imagerie were unaffected. A review of the literature since 1970 found 6 cases of an association of this type among 17 patients with visual agnosia. There appears to be no relationship between the presence of tactile agnosia and the global or partial character of the visual agnosia, the severity of memory disturbances, the presence of visuoverbal disconnection or visual imagery disorders. In contrast, these cases differed in that the lesions were more extensive and extended beyond the internal occipital regions: they were widespread in 3 cases and in the left internal occipital and parietal region in 1 case. In the patient reported in this paper there was a wide lesion of the posterior white matter of the left hemisphere.     

Hemianesthesia and aphasia. An anatomical and behavioral study

A 61-year-old right-handed man with a history of lacunar cerebrovascular disease and hypertension had the sudden onset of right-sided numbness and difficulty speaking. Neurologic evaluation revealed a dense right hemianesthesia that included the face, trunk, arm, and leg. Neuropsychological examination documented a conduction aphasia, which resolved nearly completely several months later. Computed tomographic and magnetic resonance imaging studies showed a lesion in the left hemisphere that involved the posterior insula and disrupted thalamocortical connections but entirely spared the thalamus proper. We suggest that the combination of hemianesthesia and aphasia indicates a white matter lesion subjacent to inferior parietal and posterior temporal cortices.     

Ideomotor apraxia without aphasia and aphasia without apraxia: the anatomical support for a double dissociation.

This study aimed to verify the existence of a double aphasia/apraxia dissociation. Apraxic patients without aphasia and aphasic patients without apraxia were included in a consecutive series of patients with cortical or subcortical CT documented vascular lesions in the left hemisphere. Of 699 patients, 10 were found to be apraxic but not aphasic and 149 aphasic but not apraxic. These findings indicate an aphasia/apraxia double dissociation. This suggests that praxis and language make use of two different, partly overlapping networks.     

Angular gyrus syndrome revisited: Acalculia,finger agnosia,right-left disorientation and semantic aphasia

Angular gyrus (Gerstmann) syndrome is classically described as finger agnosia, right-left disorientation, agraphia and acalculia in association to lesions in the left angular gyrus. Aphasia is not typically described as part of this syndrome. Here we report a 58 year old right-handed male, with an ischemic lesion to the left angular gyrus, who developed sudden loss of speech expression and comprehension, and slowly recovered over the following few weeks. After several months he showed significant improvement on his language skills with understanding logic-grammatical relationships, comparison adverbs (e.g. bigger-smaller, younger-older etc., place adverbs (e.g. over-below, on-beneath etc. and time adverbs (e.g. before-after). These language deficits are compatible with a semantic aphasia. Writing difficulties are minimal. In addition, he has important impairments in finger agnosia, right-left discrimination, and in understanding numbers, using numerical concepts, and performing arithmetical operations. We propose that left angular gyrus syndrome should be restated to include acalculia, finger agnosia, right left disorientation and semantic aphasia. A single underlying deficit can account for the simultaneous presentation of these four clinical signs. only mild word-finding difficulties, but with substantial difficulties in     

Visual associative agnosia and optic aphasia. A single case study and a review of the syndromes.

The case is presented of a patient who showed visual naming disturbances caused by a left occipital infarction. His performance on tests of visual naming, of recognition not requiring a verbal response, and of verbal-visual matching demonstrated a wide range of qualitatively different errors, including complete inability to recognize the object, access to partial semantic knowledge, and mere name finding difficulty. On the basis of the present case and of a review of the recent literature, the clinical distinction between visual associative agnosia and optic aphasia and the relation of these disorders with the anatomical site of lesion are discussed.     

Primary progressive aphasia accompanied by environmental sound agnosia: a neuropsychological, MRI and PET study

As part of the frontotemporal dementias, primary progressive aphasia (PPA) is typically characterized by nonfluent speech with paraphasias, but there is growing evidence that also a fluent variant of PPA exists. We describe a patient suffering from PPA who adds to the broad clinical spectrum of this disorder. Moreover, we report for the first time that PPA may be associated with severe impairment in meaningful nonverbal sound recognition (environmental sound agnosia). These neuropsychological findings were found to be associated with distinct focal alterations in functional and structural neuroimaging.     

Common dimensions of visual and auditory agnosia and an explanation of the auditory recognition deficit in aphasia.

An experimental analysis of auditory recognition disturbances was performed; 81 patients with localized cerebral lesions were examined with a recognition test for meaningful sounds and with a nonverbal intelligence test (Block Design). Sensory stimulation was 5 or 15 sec for each sound. Nonverbal intelligence accounted for a considerable and significant amount of variance in recognition performance. The aphasic group was more impaired in auditory recognition than were both the other groups, i.e., patients with right or left hemispheric lesions without aphasia. The auditory recognition disturbance in the aphasic group depended to a significant extent on stimulus duration, which means a slowing down of the recognition process in aphasia. The analogies to studies on visual agnosia are striking. In both modalities, recognition depends on intellectual functioning, sensory disturbances or reduced sensory input, and the presence of aphasia.     

The significance of the study of aphasia, apraxia and agnosia at present time]

Neuropsychology initiated by the study of aphasia, apraxia and agnosia had been regarded as one division of psychiatry. This is one of the reasons why neuropsychology is minor territory in neurology. Some people say that neuropsychology seems difficult to understand, not scientific, not useful and is rather a man's taste than a medicine. I try to respond in this paper to these critics by way of analyzing our own cases while insisting on the today's importance of the study of aphasia, apraxia and agnosia. Our personal cases consist of the following three categories. 1) Primary progressive apraxia: proposal of the symptomatic concept suggested by the investigation of our own eight cases and those in the literature. 2) Musical alexia with agraphia in a trombone player: study of the cerebral localization in a person with special ability. 3) Disturbance of reaching proposal of intracerebral pathways in kinesthesia. Therefore it is highly possible that the significance of the study of aphasia, apraxia and agnosia should become enlarged now and after; and it seems urgent to answer its need that younger neurologists participate in this area.     

A study of measles encephalitis with focal changes on MRI, auditory agnosia and expressive aphasia

Acute measles encephalitis is a typical parainfectious encephalitis in which the brain is diffusely affected clinically and neuropathologically. We present here a 5-year-old case of measles encephalitis with intractable seizures, bitemporal MRI abnormalities, and neurological sequelae of auditory agnosia and aphasia. Pathophysiology of the focal MRI lesions and of expressive aphasia due to auditory agnosia was discussed. We stressed that the status convulsions and its ischemic effect played an important role on the development of the focal lesions rather than focal encephalitis or ADEM. In the course of auditory agnosia and acquired aphasia, the patient transiently expressed some meaningful words. The significance of this episode was discussed based on the sequential changes of symptoms and neuroimaging findings.     

"Numb, clumsy hands" and tactile agnosia secondary to high cervical spondylotic myelopathy: a clinical and electrophysiological correlation

Four patients presented with a distinctive syndrome of "numb, clumsy hand" and tactile agnosia. Myelography and computed tomographic myelography (CTM) of the cervical spine documented major spondylotic compressive lesions mainly between the C3 and C5 levels. The cortical responses of dermatomal somatosensory evoked potentials (DSEPs) revealed progressively prolonged peak latencies and progressively decreased amplitudes of early components from C6 to C8 dermatomal stimulation. In comparison, the C5 and L2 DSEPs were affected to a lesser extent. This finding suggests that high cervical cord compression may produce dysfunction of the dorsal column caudal to the direct compressive sites. In other words, the funiculus cuneatus of C6-8 cord is most affected in high cervical myelopathy. Moreover, the funiculus cuneatus is within the border zone susceptible to an overall reduction in blood flow. We conclude therefore, that ischemia secondary to cord compression is the pathophysiology resulting in this unique syndrome of "numb, clumsy hands" and tactile agnosia.     

Tactile hallucinations: conceptual and historical aspects.

A brief historical analysis of the general concept of hallucination is presented and the suggestion is made that it emerged as the unwarranted generalisation of a perceptual model that was meant to apply only to vision and the "distance senses". Against this background the evolution of tactile hallucinations is considered and its interaction with 19th century psychological theory explored. It is concluded that tactile hallucinations are sui generis phenomena which do not fit the conventional model and whose clinical identification rests on criteria so far unclear. A brief review of their taxonomy and diagnostic usefulness is presented. Some wider implications are drawn which should be relevant to the general concept of hallucination.     

Ettlinger revisited: the relation between agnosia and sensory impairment.

The concept of agnosia as a higher order functional impairment, which can occur in the absence of low level visual perceptual deficits, continues to provoke debate. This controversy is complicated by the fact that, on close examination, agnosic patients do tend to have some perceptual difficulties. Thus the issue centres around the question as to whether these deficits play a causal part in the aetiology of agnosia or whether they are functionally independent, with both impairments resulting from the substantial cerebral lesions involved in agnosia. In 1956, Ettlinger published a study in which he compared the performance of patients with visual recognition deficits and patients with posterior brain lesions whose recognition abilities were intact. He argued that visual perceptual problems could not explain the recognition deficit in agnosia as he saw far worse perceptual impairments in patients who did not experience any problems in visual recognition. Although the logic of Ettlinger's argument is not disputed, some criticisms have arisen concerning the study, such as the fact that his experimental group did not include a truly object agnosic patient. In addition, Ettlinger's visual-sensory assessment can no longer be considered comprehensive in the light of present day knowledge of the cerebral visual apparatus. This study therefore investigated three (prosop)agnosic patients and five patients with unilateral brain lesions without recognition deficits on an extensive battery of visual sensory tests. The results support Ettlinger's original claim that (in some cases) agnosia cannot be explained as resulting from lower level visual impairments.     

Clinical, cognitive and anatomical evolution from nonfluent progressive aphasia to corticobasal syndrome: a case report

Recent clinical and pathological studies have suggested that frontotemporal lobar degeneration (FTLD) and corticobasal syndrome (CBS) show clinical and pathological overlap. We present four years of longitudinal clinical, cognitive and anatomical data in the case of a 56-year-old woman, AS, whose clinical picture evolved from FTLD to CBS. For the first three years, AS showed a progressive speech and language disorder compatible with a diagnosis of the nonfluent aphasia variant of FTLD. At year four, 10 years after her first symptom, AS developed the classical clinical signs of CBS, including alien limb phenomenon and dystonia. Voxel-based morphometry (VBM) applied to AS's four annual scans showed progression of atrophy from the inferior posterior frontal gyrus, to the left insula and finally to the medial frontal lobe. This case demonstrates the clinical overlap between FTLD and CBS and shows that the two can appear in the same patient at different stages of the disease in relation to the progression of anatomical damage.     

Sex differences in tactile defensiveness in children with ADHD and their siblings

Tactile defensiveness (TD) is a disturbance in sensory processing and is observed in some children with attention-deficit-hyperactivity disorder (ADHD). TD has been examined in male children with ADHD and in children with ADHD without differentiating by sex. As males and females with ADHD may differ in the clinical expression of the disorder and associated deficits, the aim of this study was to examine sex differences in TD in males and females with ADHD. Non-affected siblings were also examined to investigate familiality of TD. The Touch Inventory for Elementary-School-Aged Children was administered to 47 children with ADHD (35 males, 12 females; mean age 9y 8mo [SD 1y 11mo]), 36 non-affected siblings (21 males, 15 females; mean age 8y 10mo [SD 2y 4mo]), and 35 control children (16 males, 19 females; mean age 9y 5mo [SD 6mo]). Results indicated that females with ADHD displayed higher levels of TD than males with ADHD (who did not differ from control males). This suggests that TD is sex specific and may contribute to the identification of ADHD in females, thus improving diagnostic and therapeutic strength in this under-referred group. Non-affected siblings were unimpaired, regardless of sex, which suggests that TD is specific to the disorder and not part of a familial risk for ADHD.     

“Pre-semantic” cognition revisited: Critical differences between semantic aphasia and semantic dementia

Patients with semantic dementia show a specific pattern of impairment on both verbal and non-verbal “pre-semantic” tasks, e.g., reading aloud, past tense generation, spelling to dictation, lexical decision, object decision, colour decision and delayed picture copying. All seven tasks are characterised by poorer performance for items that are atypical of the domain and “regularisation errors” (irregular/atypical items are produced as if they were domain-typical). The emergence of this pattern across diverse tasks in the same patients indicates that semantic memory plays a key role in all of these types of “pre-semantic” processing. However, this claim remains controversial because semantically impaired patients sometimes fail to show an influence of regularity. This study demonstrates that (a) the location of brain damage and (b) the underlying nature of the semantic deficit affect the likelihood of observing the expected relationship between poor comprehension and regularity effects. We compared the effect of multimodal semantic impairment in the context of semantic dementia and stroke aphasia on the seven “pre-semantic” tasks listed above. In all of these tasks, the semantic aphasia patients were less sensitive to typicality than the semantic dementia patients, even though the two groups obtained comparable scores on semantic tests. The semantic aphasia group also made fewer regularisation errors and many more unrelated and perseverative responses. We propose that these group differences reflect the different locus for the semantic impairment in the two conditions: patients with semantic dementia have degraded semantic representations, whereas semantic aphasia patients show deregulated semantic cognition with concomitant executive deficits. These findings suggest a reinterpretation of single-case studies of comprehension-impaired aphasic patients who fail to show the expected effect of regularity on “pre-semantic” tasks. Consequently, such cases do not demonstrate the independence of these tasks from semantic memory.     

Polysomnographic and symptomatological analyses of major depressive disorder patients treated with mirtazapine.

OBJECTIVE: This study aimed to characterize the effects of mirtazapine on polysomnographic sleep, especially slow wave sleep (SWS) and rapid eye movement (REM) sleep, as well as its effects on clinical symptoms in patients with major depressive disorder (MDD). METHOD: Sixteen MDD patients were treated with mirtazapine 30 mg taken 30 minutes before bedtime. Polysomnographic and subjective sleep, as well as other clinical data, were collected at baseline and on Days or Nights 2, 9, 16, 30, and 58 during treatment. We used repeated measures analysis of variance, including pairwise comparison, to analyze data statistically. RESULTS: Mirtazapine administration increased total SWS and the SWS in the first sleep cycle, but not SWS in the second sleep cycle. The medication increased REM latency and the duration of the first REM episode; it also decreased the number of REM episodes. Simultaneously, mirtazapine significantly reduced wake-after-sleep onset and scores on the Athens Insomnia Scale. After patients took the medication, scores on the Hamilton Depression Rating Scale-17 (HDRS-17) decreased rapidly and continuously. The changes on the Beck Depression Inventory-II were consistent with those on the HDRS-17. The medication has a tendency to increase weight. CONCLUSIONS: Mirtazapine significantly improved sleep quality, reversed sleep markers of depression, and reduced depressive symptoms in this group of MDD patients.