Stuttering due to ischemic stroke

Acquired stuttering is a disorder of the fluency of speech. The mechanism underlying stuttering is unknown. It may occur after bilateral and unilateral cortical or subcortical brain damage. We report two cases who had stuttering resulting from left parietal infarction.     

Neurophysiology and neuroanatomy of smooth pursuit: Lesion studies

Smooth pursuit impairment is recognized clinically by the presence of saccadic tracking of a small object and quantified by reduction in pursuit gain, the ratio of smooth eye movement velocity to the velocity of a foveal target. Correlation of the site of brain lesions, identified by imaging or neuropathological examination, with defective smooth pursuit determines brain structures that are necessary for smooth pursuit. Paretic, low gain, pursuit occurs toward the side of lesions at the junction of the parietal, occipital and temporal lobes (area V5), the frontal eye field and their subcortical projections, including the posterior limb of the internal capsule, the midbrain and the basal pontine nuclei. Paresis of ipsiversive pursuit also results from damage to the ventral paraflocculus and caudal vermis of the cerebellum. Paresis of contraversive pursuit is a feature of damage to the lateral medulla. Retinotopic pursuit paresis consists of low gain pursuit in the visual hemifield contralateral to damage to the optic radiation, striate cortex or area V5. Craniotopic paresis of smooth pursuit consists of impaired smooth eye movement generation contralateral to the orbital midposition after acute unilateral frontal or parietal lobe damage. Omnidirectional saccadic pursuit is a most sensitive sign of bilateral or diffuse cerebral, cerebellar or brainstem disease. The anatomical and physiological bases of defective smooth pursuit are discussed here in the context of the effects of lesion in the human brain.     

Neurophysiology and neuroanatomy of smooth pursuit: Lesion studies

Smooth pursuit impairment is recognized clinically by the presence of saccadic tracking of a small object and quantified by reduction in pursuit gain, the ratio of smooth eye movement velocity to the velocity of a foveal target. Correlation of the site of brain lesions, identified by imaging or neuropathological examination, with defective smooth pursuit determines brain structures that are necessary for smooth pursuit. Paretic, low gain, pursuit occurs toward the side of lesions at the junction of the parietal, occipital and temporal lobes (area V5), the frontal eye field and their subcortical projections, including the posterior limb of the internal capsule, the midbrain and the basal pontine nuclei. Paresis of ipsiversive pursuit also results from damage to the ventral paraflocculus and caudal vermis of the cerebellum. Paresis of contraversive pursuit is a feature of damage to the lateral medulla. Retinotopic pursuit paresis consists of low gain pursuit in the visual hemifield contralateral to damage to the optic radiation, striate cortex or area V5. Craniotopic paresis of smooth pursuit consists of impaired smooth eye movement generation contralateral to the orbital midposition after acute unilateral frontal or parietal lobe damage. Omnidirectional saccadic pursuit is a most sensitive sign of bilateral or diffuse cerebral, cerebellar or brainstem disease. The anatomical and physiological bases of defective smooth pursuit are discussed here in the context of the effects of lesion in the human brain.     

Bilateral opercular syndrome and crossed aphemia due to a right insular lesion: A clinicopathological study

A right-handed male patient suddenly noted lower bilateral facial and lingual palsy, and inability to masticate and swallow, but with preserved automatic functions. He was mute, communicating only through writing, but verbal comprehension was normal (aphemia). On anatomopathological examination, an ischemic infarction of the entire right insula, with mild extension to the fronto-temporoparietal operculum was observed. The left hemisphere was normal. The clinical findings suggest a bilateral opercular syndrome due to a right hemisphere lesion and a crossed aphemia.     

Further lesion evidence for the neural basis of conceptual knowledge for persons and other concrete entities

The neural underpinnings of conceptual knowledge have been studied intensively, but many unanswered questions remain. In a previous study examining recognition of persons, animals, and tools in 116 participants with unilateral brain lesions, we found no instance of a patient who manifested defective recognition in all three categories. We reasoned that the spatial distribution of the lesion loci critical for the appearance of recognition defects for these different categories explained why this ‘three‐way’ defect could not be found in patients with unilateral lesions, and we proposed that only a suitable bilateral lesion would be likely to produce such a combined defect. In the study reported here, we tested this hypothesis by investigating recognition performances in 55 participants with bilateral cortical lesions. In support of the hypothesis, nine patients, all of whose lesions included bilateral occipitotemporal and/or temporal cortices, had a three‐way recognition impairment (persons, M=18.3%; animals, M=35.7%; tools, M=71.3%; all scores >2 SDs below normal). As expected, bilateral lesions to other neural sectors, for example prefrontal cortices, did not lead to recognition impairments. These findings provide further support for the notion that retrieval of knowledge for concrete entities from different conceptual categories depends on partially segregated neural systems, located in different sectors of occipitotemporal and temporal regions in right and left hemisphere.     

The neuropsychology of paramedian thalamic infarction

A longitudinal study of three patients with CT-scan documented paramedian thalamic infarctions (bilateral, primarily right, unilateral left) is reported and the neuropsychology of human paramedian thalamic infarction is reviewed. The neuropsychological deficits following these selected lesions, the nature of the clinical memory disorder, and the neuroanatomy of memory are discussed. The significance of cortical/subcortical relationship in explaining observed behavioral changes is emphasized. Brain damage with maximum involvement in the dorsomedial nuclei and mamillothalamic tracts appears to cause primarily a memory disorder and frontal-limbic behavioral changes, the severity and profile of deficits depending on lesion extent and location. Both anterograde and remote memory loss may be present. Asymmetry in memory at the level of the thalamus was observed, following the left-verbal, right-nonverbal dichotomy.     

Brain activity varies with modulation of dynamic pitch variance in sentence melody

Fourteen native speakers of German heard normal sentences, sentences which were either lacking dynamic pitch variation (flattened speech), or comprised of intonation contour exclusively (degraded speech). Participants were to listen carefully to the sentences and to perform a rehearsal task. Passive listening to flattened speech compared to normal speech produced strong brain responses in right cortical areas, particularly in the posterior superior temporal gyrus (pSTG). Passive listening to degraded speech compared to either normal or flattened speech particularly involved fronto-opercular and subcortical (Putamen, Caudate Nucleus) regions bilaterally. Additionally the Rolandic operculum (premotor cortex) in the right hemisphere subserved processing of neat sentence intonation. As a function of explicit rehearsing sentence intonation we found several activation foci in the left inferior frontal gyrus (Broca's area), the left inferior precentral sulcus, and the left Rolandic fissure. The data allow several suggestions: First, both flattened and degraded speech evoked differential brain responses in the pSTG, particularly in the planum temporale (PT) bilaterally indicating that this region mediates integration of slowly and rapidly changing acoustic cues during comprehension of spoken language. Second, the bilateral circuit active whilst participants receive degraded speech reflects general effort allocation. Third, the differential finding for passive perception and explicit rehearsal of intonation contour suggests a right fronto-lateral network for processing and a left fronto-lateral network for producing prosodic information. Finally, it appears that brain areas which subserve speech (frontal operculum) and premotor functions (Rolandic operculum) coincidently support the processing of intonation contour in spoken sentence comprehension.     

Effects of lesions of the central nucleus of the anterior archistriatum on contact call and warble song production in the budgerigar (Melopsittacus undulatus)

We studied the effects of both unilateral and bilateral lesions of the central nucleus of the anterior archistriatum (AAc) on the production of contact calls and warble song in adult male and female budgerigars. Birds were sorted into three experimental groups based on the percentage of AAc destroyed and whether lesions were unilateral or bilateral. The experimental groups were Unilateral Lesion (N = 8), Partial Bilateral Lesion (N = 5), and Bilateral Lesion birds (N = 12). Each group contained both sexes. Unilateral lesions had no demonstrable effects on contact call or warble song production. Bilateral lesions resulted in immediate and permanent disruption of all learned temporal and spectral characteristics of contact calls, although call initiation was not dependent on the AAc. Partial bilateral lesion effects varied with lesion size and location. At least 20-30% sparing of the AAc, including sparing portions of both the dorsal (AAcd) and ventral (AAcv) subdivisions on the same side of the brain, is necessary for production of prelesion contact call patterns. Warble song was absent in birds with complete bilateral destruction. Two birds with large yet incomplete lesions of the AAc sang after surgery, although the warble song of these birds was extremely impoverished and contained only a few of the typical warble song elements. Lesion results indicate that the AAc mediates the production of learned vocal features in male and female budgerigars, with each hemisphere capable of supporting a normal vocal repertoire.     

Frontal-opercular aphasia.

The standard nomenclature divides nonfluent aphasic syndromes with relatively spared comprehension into Broca's aphasia and transcortical motor aphasia. We report on a patient with a persistent nonfluent aphasia from a discrete, primarily cortical, frontal-opercular lesion who had impaired syntax but intact repetition and, therefore, did not conform to the traditional classification. Based on this patient's behavior and a review of other cases, we have divided the nonfluent aphasias with intact comprehension into five disorders. (1) Verbal akinesia-exhibiting diminished intention or drive to speak and associated with medial frontal lesions (supplementary motor area and cingulate gyrus) or with lesions damaging the efferent projections from these areas. (2) Disorders of syntax-telegraphic and agrammatic utterances that may be associated with dominant pars opercularis lesions. (3) Phonemic disintegration-a failure to correctly produce phonemes, which may be associated with injury to the opercular primary motor cortex or efferent projections from this area. (4) Defects of lexical access-patients who struggle to find words and are impaired at timed word-generation tasks. Defects of lexical access may be associated with lesions of the pars triangularis and adjacent prefrontal cortex. (5) Mixed defects. According to this model, the traditional patient with Broca's aphasia would exhibit disorders of syntax, phonemic disintegration, and defects of lexical access, whereas the traditional patient with transcortical motor aphasia would have verbal akinesia or defects of lexical access or both. Our patient had defects of lexical access and syntax, but only mild symptoms of phonemic disintegration, suggesting that his opercular primary motor cortex was relatively intact. Our patient's ability to repeat normally while his propositional speech remained telegraphic suggests that different neural mechanisms subserve these functions.     

Anton's syndrome following callosal disconnection

Anosognosia for cortical blindness, also called Anton's syndrome, is a rare neurological disorder usually following bilateral lesions to occipital cortices. Neuropsychological, morphological and functional neuroimaging (SPECT and fMRI) findings are reported in a patient who incurred Anton's syndrome after an ischaemic lesion confined to the left occipital lobe involving the corpus callosum. The present case study suggests that Anton's syndrome may also follow from lesions disconnecting the occipital cortices.     

Neural substrates of word generation during stroke recovery: the influence of cortical hypoperfusion

Several studies have demonstrated reorganization of cognitive and motor function caused by stroke. This study examined the influence of hypoperfused brain regions, in addition to the area of the infarct itself, on reorganization of the cognitive processes underlying word generation in stroke patients. In addition, we also sought to determine the influence of hypoperfusion on the blood oxygen level dependent/(BOLD) effect. Subjects with left and right subacute or chronic subcortical strokes, along with normal controls, were imaged while performing a verbal fluency task (word generation). The study population included six normal subject and six stroke patients with subcortical infarcts and cortical hypoperfusion in the middle cerebral artery territory who had recovered or improved markedly in word fluency. While normal subjects displayed a left-lateralized fronto-temporo-parietal and bilateral cingulo-striatal-thalamic-cerebellar network, the activation pattern of stroke patients was determined both by the hypoperfused regions and infarcted areas of the brain. Specifically, patients showed diminished BOLD effect in the cortical regions that were hypoperfused, even though their infarcts were subcortical, and showed increased BOLD effect in the homologous regions of the normal hemisphere. This finding raises the possibility that cortical hypoperfusion in the absence of infarct can cause shift of language functions to the opposite, intact hemisphere. However, reduced BOLD effect in the task relative to rest was found in hypoperfused regions in two patients, raising the possibility that regional function persisted, even though vascular reactivity was impaired. Results illustrate the complexities of functional imaging studies of recovery in patients with vascular lesions.     

Basal ganglia participation in language pathology

Language disturbances were studied in 40 patients with well-demarcated vascular lesions of the speech-dominant hemisphere. Computerized cranial tomography was used for localization of the lesion. Special emphasis was given to the analysis of automatized speech and repetitive verbal phenomena.Subcortical infarctions with basal ganglia involvement led to transient aphasia although long-lasting abnormalities of language could be detected in these patients. Aphasia was more severe if a cortical lesion was combined with a basal ganglia lesion. Automatisms and recurring utterances occurred only with combined cortical and basal ganglia lesions. A lesion of Wernicke's area alone, without involvement of prerolandic structures or subcortical nuclei, was sufficient to produce long-lasting aphasia, whereas lesions of Broca's area alone produced only transient language disturbances. The results are compatible with a recent theory of multiple cerebral representation of function.     

Mutism associated with buccofacial apraxia and bihemispheric lesions

Mutism following brain trauma is quite common, is usually transient, and recovery of speech is essentially the rule. Lasting total absence of speech without aphasia is highly unusual. Three such patients, two of traumatic and one due to vascular origin showing buccofacial apraxia (BFA) and computerized tomography (CT) evidence of bilateral frontal lesions are reported. It is suggested that complete lasting mutism associated with BFA is a result of bihemispheric lesions affecting mainly the opercular part of the inferior frontal gyrus and immediate adjacent regions.     

Unilateral brain lesions in childhood: performance on the Revised Token Test

Comprehension of connected language as assessed by the Revised Token Test (RTT) was studied in 17 children with left hemisphere lesions (LL) and 11 with right hemisphere lesions (RL). LL children's significantly lower performance on several subtests than left controls (LC) matched by age, sex, race, and social class appeared to be related to the memory demands of these subtests rather than the limited syntactic elements assessed by the RTT. LL subjects requested significantly more command repetitions than control or RL subjects and when a repetition was not requested LL subjects often responded with immediacy. Although RL children tended to perform lower than right matched controls (RC), these differences were not significant nor readily related to either the memory or specific linguistic structures assessed. RL subjects required fewer command repetitions than LL subjects and exhibited a significantly greater frequency of immediate responses than controls or LL subjects. While based on few children, a trend for LL children with retrorolandic lesions to perform more poorly than those with left prerolandic lesions was suggested. No systematic difference in performance was apparent for children with left cortical vs. left subcortical lesions or among discrete sites of lesions within the right hemisphere. Children with left lesions prior to 1 year of age performed no better and, in several instances, significantly poorer than LL patients sustaining lesions after 1 year of age. Among RL subjects, those sustaining lesions after 1 year of age had greater difficulty than those with lesion onset before 1 year of age, especially on linguistic elements which seemed to be dependent upon visual spatial properties. Further studies are needed to evaluate the comprehension of more complex linguistic structures among children with unilateral brain lesions as well as to study the role of more basic factors such as memory and attention in explaining the present findings.     

Neural substrates of the ‘low‐level’ system for speech articulation: Evidence from primary opercular syndrome

We describe a patient with progressive disorder of speech, without language impairment (opercular syndrome). Morphometric analysis confirmed asymmetric volume reduction of the precentral areas (>left). Diffusion imaging showed significant white matter changes in the left frontal lobe, with specific involvement of the left corticobulbar tract and connections between supplementary/pre‐supplementary motor areas and the frontal operculum (frontal aslant tract). We suggest that the organization of expressive language includes a ‘low level’ motor system principally distributed in the left hemisphere that shows specific susceptibility to neurodegeneration, distinct from neural systems subtending praxic, and cognitive aspects of language.     

Opposed left and right brain hemisphere contributions to sexual drive: a multiple lesion case analysis

Brain topographical studies of normal men have have shown that sexual excitation is asymmetric in the brain hemispheres. Group studies of patients with unilateral epileptic foci and other studies of patients with unilateral brain lesions have come to the same conclusion. The present study reviewed previously published single case reports of patients with frank hypo or hypersexuality subsequent to a unilateral brain lesion. Hyposexual patients tended to have left hemisphere lesions (primarily of the temporal lobe), and hypersexual patients tended to have right hemisphere lesions (primarily of the temporal lobe) (p < 0.05). We interpret this double dissociation as part of a more general phenomenon of psychic tone similarly dissociated with regard to hemispheric control, including mood, psychomotor baseline, speech rate, and even immunity. The behavioral significance of this psychic tone is to modulate approach versus avoidance behavior.     

Impaired shifting of attention in Balint's syndrome

We assessed the efficiency of attentional shifts across the horizontal and vertical axes of the visual field in a patient with Balint's syndrome caused by bilateral parieto-occipital infarctions. This was performed using an adaptation of Posner's peripheral cueing paradigm. In contrast to normal controls and patients with unilateral parietal lesions previously reported, this patient did not benefit from cues directing attention to the left or right visual field. She appeared to benefit only when the cues directed attention to the upper visual field. This suggests a defect in shifting attention that may occur following bilateral parietal lesions. We discuss the implications of these findings for the role of the parietal lobes in attentional processes and for our understanding of the behavioral abnormalities observed in Balint's syndrome.     

Neural systems for recognition of emotional prosody: a 3-D lesion study

Which brain regions are associated with recognition of emotional prosody? Are these distinct from those for recognition of facial expression? These issues were investigated by mapping the overlaps of co-registered lesions from 66 brain-damaged participants as a function of their performance in rating basic emotions. It was found that recognizing emotions from prosody draws on the right frontoparietal operculum, the bilateral frontal pole, and the left frontal operculum. Recognizing emotions from prosody and facial expressions draws on the right frontoparietal cortex, which may be important in reconstructing aspects of the emotion signaled by the stimulus. Furthermore, there were regions in the left and right temporal lobes that contributed disproportionately to recognition of emotion from faces or prosody, respectively.     

Change of perspective in discourse comprehension: encoding and retrieval processes after brain injury

Damage to frontal areas has been associated with nonaphasic language disturbances in which word and sentence level processes remain largely intact but text level processes are impaired. Most studies providing evidence for these language deficits have concentrated on text production. To study text comprehension of nonaphasic patients, we adopted the paradigm of Anderson and Pichert (1978) that was developed to separate encoding from retrieval processes. Subjects read a story under one of two alternative perspectives and subsequently recalled it. After this first recall, they were instructed to now adopt the second perspective and to recall the story once more. Twenty-four brain-injured patients participated. Each patient's lesion was evaluated with respect to the involvement of right- and/or left-frontal regions. Seven patients showed unilateral left-frontal lesions, five patients unilateral right-frontal lesions, four patients had bilateral frontal damage, and the lesions of the remaining eight patients did not involve frontal areas. The only factor predicting behavioral results was the presence of a left-frontal lesion. For patients without frontal lesions and patients with unilateral right-frontal lesions, we replicated previously reported results. Encoding relevant information was recalled better than other information. Furthermore, the switch of perspective aided recall of perspective relevant information during the second recall. In contrast, patients with left-frontal or bilateral frontal lesions could not make use of the perspective instructions. While they showed comparable recall performance, as well as sensitivity to the relative ease of information, neither the encoding instructions nor the switch instructions had an impact on the recall patterns. These results suggest that left-frontal damage leads to an impairment of goal directed text processing skills.