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A detailed acoustic analysis was conducted of the speech production of a single patient presenting with the foreign accent syndrome subsequent to a left-hemisphere stroke in the subcortical white matter of the pre-rolandic and post-rolandic gyri at the level of the body of the lateral ventricle. It was the object of this research to determine those changes which contribute to the perception of a "foreign accent." A number of acoustic parameters were investigated, including features of consonant production relating to voice, place, and manner of articulation, vowel production relating to vowel quality and duration, and speech melody relating to fundamental frequency. The results indicated that many attributes which might have contributed to the foreign quality of the patient's speech were similar to those of normal English speakers. However, a number of critical elements involving consonant and vowel production and intonation were impaired. It was hypothesized that the acoustically anomalous features are linked to a common underlying deficit relating to speech prosody. It is suggested that the normal listener categorizes this speech pattern as a foreign accent because the anomalous speech characteristics, while not a part of the English phonetic inventory, reflect stereotypical features which are a part of the universal phonetic properties found in natural language.

We have analysed the aphasia profiles of 19 cases with subcortical infarction or haemorrhage. Several components of the aphasic syndromes, especially sentence length and grammatical form (together compromising fluency), ease of speech initiation, articulation, voice volume, and auditory comprehension, were individually isolated for correlation with CT lesion site. Each component had a specific lesion site correlation, and lesions in various deep periventricular white matter regions were the critical ones for all components of aphasia. Simple tabulation of lesions as cortical or subcortical, and restricting analysis to lesions of basal ganglia would both have proved inadequate to account for clinical findings. A review of 61 subcortical cases in the neurological literature for which CT and aphasia data were available supports these conclusions.

We have demonstrated that the deficit in speech perception in our patient with pure word deafness is secondary to a prephonemic temporal auditory acuity disorder. We delineated the nature of the auditory processing deficit in our patient with bilateral lesions and then demonstrated the presence of a predicted deficit in phonemic discrimination. This pattern is comparable to previous cases with bilateral lesions and distinct from other cases with unilateral lesions. Review of previous reports suggests that there are two distinct types of pure word deafness: type 1, in which the deficit is prephonemic and related to a temporal auditory acuity disorder, and type 2, a form that is independent of a temporal auditory acuity disorder, and has a deficit in linguistic discrimination that does not adhere to a prephonemic pattern (Denes and Semenza, 1975; Saffran et al., 1976). The former has been associated with bilateral temporal lobe lesions (Naeser, 1974; Chocholle et al., 1975), the latter with left unilateral lesions (Denes and Semenza, 1975; Saffran et al., 1976). The first form is an apperceptive disorder, whereas the second represents a higher disorder in phonemic discrimination and may be considered a fragment of Wernicke's aphasia.

• Two patients with transcortical motor aphasia are described. Both had infarcts in the distribution of the left anterior cerebral artery confirmed by computerized tomography (CT). The distinctive language abnormality, unusual EEG pattern, and nuclide and CT scan abnormalities all allow ready diagnosis of the syndrome of infarction in this distribution. The mechanism of the language disturbance is reviewed and implications for treatment and prognosis are discussed.

• Six patients had ischemic infarcts in the paramedian thalamic, subthalamic, and mesencephalic areas. In addition to ocular motility problems, ataxia, dysmetria, and mild pyramidal signs, there were consistent behavioral observations and neuropsychological findings. All of the patients had initial deficits in arousal, and gradually improved to normal wakefulness. When awake, all of the patients had impaired attention, mental control, and slowed verbal and motor responsiveness. They were apathetic, poorly motivated, and affect was flat or occasionally labile. All of the patients had a memory disorder characterized by anterograde and retrograde loss. One patient had significant language impairment. These deficits persisted in all but one patient who had a predominantly mesencephalic lesion. We believe the cluster of findings in these patients constitutes a characteristic syndrome of dementia related to paramedian mesencephalic and diencephalic infarcts. This syndrome bears close resemblance to that associated with some subcortical degenerative disorders such as progressive supranuclear palsy. In cases of paramedian mesencephalic and diencephalic infarcts, however, computed tomography and magnetic resonance imaging can delineate clinicoanatomic relationships that account for specific constituents of the syndrome.

A patient with pure alexia was presented with a series of tachistoscopic tests involving words, letters, pictures, and lines. Low level perceptual processing remained intact. A major deficit was revealed in the speed of identifying orthographic material. This deficit extended to the identification of pictures presented at tachistoscopic durations, although no disturbance in the visual identification of pictures or objects was observed in real time. There were frequent reports of visual imagery associated with the perception of written material. These images cannot account for the patient's partial recovery of reading functions; instead, it appears that the abnormal characteristics of the patient's reading arise because, after a visual stimulus is perceived, an abnormally long period of time is required before the patient can identify the stimulus. It is suggested that pure alexia is the behavioral manifestation of a deficit in speed of visual identification which is not specific to orthographic m...

The position of the auditory pathways in the human corpus callosum has not been defined by modern imaging techniques. We report a case with a discrete hemorrhagic lesion in the posterior body of the corpus callosum. The only signs of disturbed callosal function were limited to the auditory system--suppression of left ear stimuli with dichotic listening and neglect of left-sided auditory simultaneous stimuli.

In a short examination for dysphasia six language skills should be tested: spontaneous speech, repetition, naming, comprehension of spoken language, reading, and writing. The following examination can be completed in 10–15 minutes at the bedside.

Language is a means by which people communicate with each other using verbal symbols. Dysphasia may be defined as a disorder of language due to brain damage. This monograph deals with disorders of language, not disorders of speech. Speech refers to the mechanical process of articulation, which can be disturbed by weakness, slowness, or incoordination of the muscles of the glossopharyngeal apparatus. Such disturbances would be termed dysarthria, dysphonia, or mutism. The term dysphasia is applied to a neurological disorder resulting from damage to those regions of the cerebral hemispheres which form the anatomical basis for the human capacity for language.

Aphasiologists are no longer satisfied with impressionistic judgements as to the effectiveness of dysphasia rehabilitation. Instead they seek scientific evidence, through formal studies, that treatment has a significantly positive effect on dysphasic patients. When undertaking any treatment study, certain variables which may confound the results must be identified and controlled. The most potent of the variables to be considered in dysphasia rehabilitation is the phenomenon known as spontaneous recovery. This is the period during which structurally undamaged portions of the brain regain function following insult. If treatment is administered during the period of natural recovery, then the investigator has the task of differentiating effect of treatment from effect of spontaneous improvement. There is, however, little agreement as to exactly how long spontaneous recovery takes place. Vignolo (1964) retrospectively examined the evolution of dysphasia in 69 non-traumatic patients and found that patients seen after 2 months had only a limited possibility of spontaneous recovery compared to patients seen before 2 months. Culton (1969) studied the recovery patterns of 21 dysphasics and concluded that the greatest degree of recovery takes place in the first month post onset, and that little more occurs after 2 months. Butfield and Zangwill (1946) and Luria (1963), on the other hand, State that spontaneous recovery takes place for as long as six months, particularly in traumatic dysphasias. Other authors use a 3 month cut off point (Sarno and Levita, 1971). Despite the disagreement as to the length of the spontaneous recovery period, the phenomenon is real, and must be reckoned with in any dysphasia treatment study.

In pure alexia, acquired inability to read contrasts with normal speech and handwriting. Rare cases of right hemisphere lesions causing this syndrome are usually attributed to right hemisphere dominance for language. After infarction of the right occipital lobe and thalamus, a fully right-handed man became allelic, but language and spontaneous and dictated writing were intact. Left hemispatial neglect and constructional disturbances were marked, and we suggest that pure alexia was mimicked by the impairment in visuospatial perception. Injury of the no dominant hemisphere and thalamus together may have been important in causing these deficits.

We studied 9 patients with severe, chronic Parkinson disease and complications of long-term L-DOPA therapy. After a "holiday" of 3 to 21 days, excess dopamine effects improved in all patients, and the baseline parkinsonian picture emerged. After reinstitution of L-DOPA therapy, often at lower doses than had been used previously, parkinsonian signs improved. Complications of immobility were seen in two patients; one had deep vein thrombophlebitis, and the other became depressed. In treating the individual patient, the risks of immobility despite aggressive attempts to prevent complications should be weighed against the possible improvement of parkinsonism. These findings suggest that a holiday from L-DOPA therapy may extent the drug's usefulness in treating Parkinson disease, perhaps by resensitizing striatal dopamine receptors in patients receiving the drug for prolonged periods.

Numerous theories discuss the neuropsychological functions of the frontal lobes, most based on some concept of supramodality, and an extensive literature presents the phenomenology and semiology of language and communication deficits after focal brain lesions involving the frontal lobes. Despite this, few attempts have been made to link the clinical phenomenology to a theory. This paper presents (1) a general theory of frontal functions; (2) a brief summary of experimental and anatomical literatures in support of defined frontal functional systems; (3) clinical observations that delineate these functional systems for the specific modalities of language and communication; (4) a review of the available literature supporting the idea of specific modal and supramodal language and communication capacities; (5) hypotheses about the distributed anatomy of these functional systems; and (6) implications for traditional clinical notions of aphasia, particularly in relation to a general theory of frontal lobe functions.

Speech pathologists are called upon to rehabilitate adults with disorders which range from global dysphasia with severe impairment in all language modalities, to anomic dysphasia with impairment only in substantive word finding. There is little reason to expect that disorders which vary widely in nature should or can be treated in a similar manner. There are, of course, some general principles which can be applied to any rehabilitative process and dysphasia is no exception. Such clinicians as Backus (1937) and Schuell, Jenkins and Jimeniz-Pabon (1964) provide us with general principles of treatment, and these principles are no less appropriate today than when they were written. Few of us would dispute, for example, that speech processes operate with greater facility when the individual experiences a reasonable degree of social adequacy (Backus, 1937), or that the clinician should elicit and not force the response (Schuell, Jenkins and Jimenez-Pabon, 1964). But while such principles may guide us in the treatment process, we must have a specific method in mind when sitting across from the patient.

• We examined four patients with transcortical sensory aphasia and eight with milder language disturbances but with similar thalamic and/or temporo-occipital lesions. Specific attention was paid to differentiation of the computed tomographic lesion site of the milder cases from the transcortical sensory aphasia cases. The critical lesion for transcortical sensory aphasia in these patients involved pathways in the posterior periventricular white matter adjacent to the posterior temporal isthmus, pathways that are probably converging on the inferolateral temporo-occipital cortex. Analysis of the language function of these patients, of the influence of sensory modalities on language function, and of the interaction between semantic memory and semantic lexical functions suggests the existence of a specific brain system for semantic functions. This semantic system has a particular distributed anatomy. We propose that damage to this system may have a variety of clinical manifestations in language and in memory, depending on the exact lesion configuration.

• Nine cases of subcortical aphasia with capsular/putaminal (C/P) lesion sites demonstrated on computed tomographic (CT) scans were studied. Eight cases were occlusive-vascular in etiology and one was hemorrhagic. Three subcortical aphasia syndromes and three C/P lesion site patterns were observed. Patients with C/P lesion sites with anterior-superior white-matter lesion extension had good comprehension, grammatical, but slow, dysarthric speech, and lasting right hemiplegia. Patients with C/P lesion sites with posterior white-matter lesion extension across the auditory radiations in the temporal isthmus had poor comprehension, fluent Wernicke-type speech, and lasting right hemiplegia. Patients with C/P lesion sites with both anterior-superior and posterior extension were globally aphasic and had lasting right hemiplegia. Although these cases of C/P subcortical aphasia shared certain well-known features of Broca's and Wernicke's cortical aphasia syndromes, they did not completely resemble cases of either Broca's, Wernicke's, global, or thalamic aphasia in neurologic findings, CT scan lesion sites, or language behavior. Further study of the subcortical aphasias associated with these C/P lesion sites seems to be warranted.

• Hospital records of 53 children and adolescents, aged 18 years or less, with closed head injury were reviewed for information on long-term outcome. Computed tomographic scans were used to divide the patients into clinicopathologic groups. Within these groups, duration of coma was the major index of severity. Outcome was assessed using the Glasgow Outcome Scale and by evaluating social behavior, school performance, and vocational functioning. Patients with diffuse injury plus focal lesions fared worse than those with diffuse injury only. Coma lasting more than one month led to a poorer outcome in both groups. Many individuals had limiting emotional disturbances, which may have resulted from disruption of frontal systems modulating arousal and social behavior.

The formal, clinical assessment of dysphasia encompasses at least five aspects. Depending on the circumstances, all may be given equal weight, one may be dominant to the exclusion of all the others, or any distribution of emphasis between these extremes may obtain. These aspects are the following: 1. dysphasia testing as an inventory of language input and Output modalities, 2. linguistic aspects, 3. diagnostic aims, 4. the dysphasia examination as a case study, 5. quantitative aspects.

We describe a brain-damaged patient who produced two distinctive forms of confabulation, typical and atypical (aphasic), both of which were associated with perseveration, poor self-monitoring, and denial of deficit. We propose that the typical confabulations are triggered by gaps in memory for the period surrounding the onset of his illness, while the aphasic (fantastic) confabulations are triggered by gaps in semantic representation. These observations suggest that confabulations may comprise a portion of the language deficit in patients with other varieties of fluent aphasia.

Two patients with severe amnesia following rupture of anterior communicating artery aneurysms were able to learn a complex algorithm for mentally squaring two-digit numbers. Although both patients learned the algorithm at a similar rate, one patient's improvement was accounted for by savings in the steps of the algorithm. The other patient, however, showed little improvement in the steps while performance of the whole algorithm improved dramatically. Neither patient showed savings in the Hebb Digit Span procedure. The results suggested a dissociation between amnesics in their capacity to learn the constituent “productions” or steps of a skill and their capacity to organize those productions into a single coherent act.

• Solitary plasmacytoma Invaded the petrous bone of a patient, and produced multiple cranial neuropathies. To our knowledge, this tumor has not previously been reported to cause this syndrome.

Individual cases of crossed aphasia (aphasia after a right hemisphere lesion in a right-hander) have often been reported. A number of theories have been proposed as to the neuropsychological and/or nerobiological mechanisms that might underlie this phenomenon, but there is still disagreement about its language phenomenology and possible significance. We report 2 cases of crossed aphasia after stroke and review 34 cases from the literature with anatomical documentation of lesion site. Analysis of this material suggests that they represent at least two populations. There may be general conclusions concerning mechanisms of cerebral lateralization to be learned from the investigation of anomalous groups such as crossed aphasics.

A review of early accounts of dysphasia (Benton and Joynt, 1960) credits Valerus Maximus in 30 A.D. with the earliest description of acquired dyslexia: a case of head injury producing an isolated acquired dyslexia. After an interval of almost two millenia, sporadic reports of acquired dyslexia became more common in the 1800’s but definitive steps toward understanding the acquired disorders of written language were not made until Dejerine (1891, 1892). His descriptions of the clinical findings and anatomical correlations of acquired dyslexia, with and without dysgraphia, remain essentially unaltered as the foundation of the study of disorders of written language.

We describe five patients with spontaneous, persistent confabulation. While the basis of confabulation in general is not known, the evidence in this specific group of patients with spectacular, impulsive, and spontaneous confabulation suggests a marked deficit in frontal function, superimposed upon a basic defect in memory, as a possible mechanism.

We studied 11 patients with amnesia and personality change after surgical repair of ruptured anterior communicating artery ( ACoA ) aneurysm. CT and clinical evidence suggested that infarction in the territory of the ACoA was responsible for amnesia and personality change. The medial septal nuclei, the paraventricular nucleus of the anterior hypothalamus, and the medial forebrain bundle are the primary areas of potential interest in these cases. Gross infarction in the frontal lobes is not a requirement for the syndrome.

We studied eight children with acquired aphasia. All had left hemisphere lesions. In most, the correlation between the CT lesion site and the resulting aphasic syndrome duplicated an anatomic-clinical correlation described in adults. Rapid recovery of language fluency distinguished the children from reported adults. Late follow-up indicated poor scholastic achievements, reflecting an acquired handicap in new learning. Anatomic-clinical correlates and recovery patterns suggest that brain organization for language is similar but not identical in children and adults.

• We present a case of progressive bulbar paresis in a 2-year-old child, with appropriate autopsy findings. A review of previously reported cases and a comparison with more extensive literature in Werdnig-Hoffmann disease suggest that Fazio-Londe disease is not unique, but belongs in the spectrum of progressive lower motor neuron disease.

The preceding short examination for dysphasia can be used to provide a rough clinical guide to Classification of dysphasic syndromes. Formal language evaluation should be carried out to refine the initial impression. We emphasize that many patients with dysphasia do not have signs which can be easily or neatly categorized, regardless of the technical skill or years of experience of the examiner; in such cases a thoughtful description of the Observation is more helpful than an attempt to force the clinical findings to conform to a pre-conceived category.

It is traditional that a review of the anatomy of language disorders commences with a summary of the history of the disputes between the proponents of the two main streams of thought about brain-language relationships. The ebb and flow of popularity of various localizationist and globalist theories is colorful and instructive, but it is well reviewed elsewhere (Hecaen and Albert, 1978). This issue is no longer relevant in the sense considered by previous generations. Clearly brain functions are not equally represented in all regions. Interhemispheric differences exist in 1) the perception and manipulation of higher level sensory information, 2) the Organization of axial, limb and buccofacial movements and 3) the ability to generate speech and language. These interhemispheric differences are based in part on anatomical asymmetries which are evident in fetal life (Wada et al., 1975). There is intrahemispheric specialization in brain function as well, and within the left hemisphere, much of this specialization in function constitutes the anatomy of language. Even many ostensible critics of the localizationist theories resorted to a system of language Classification that carried implicit functional localization which strongly resembled the classical formulations of Wernicke (1874) and Dejerine (1914). For example, Marie (1917), Head (1926), and Goldstein (1948), despite their reputations as antilocalizationists, utilized systems of Classification based on functional anatomy.

Syndromes of dysphasia may vary from the forms described in the preceding sections, or certain aspects of dysphasic syndromes may appear more prominently than others, depending on associated clinical conditions, language background of the patient, history of left-handedness, lesion localization, or individual differences. In this section we consider clinical features of some of these special forms of dysphasia.

The Syndrome of Broca’s dysphasia often evolves over a period of months and sometimes years from an initial stage of global dysphasia, but may occasionally appear in its own right as an acute dysphasia. In the completely developed picture of Broca’s dysphasia, spontaneous speech is nonfluent and agrammatic, while auditory comprehension is preserved at levels adequate for understanding most conversation and even at nearly normal levels in some patients. Sentence repetition is seriously impaired, although repetition of one- or two-word segments may be possible. Writing is usually on a par with speech. Reading aloud parallels the limited Output of spontaneous speech but reading for meaning, though sometimes slow and painstaking, is usually preserved at the level of auditory comprehension. Naming on visual confrontation is often slightly superior to the ability to generate names in spontaneous speech or in response to word definitions. Right hemiparesis affecting the arm more than the leg, buccofacial apraxia, and ideomotor apraxia of the motorically spared left Upper extremity are common. In the acute stage, if the initial deficit of auditory comprehension is mild, disturbances of writing are minimal and hemiparesis is not marked, and rapid improvement from a State of severe nonfluency is to be expected over several days or weeks. In these latter patients, agrammatism, as measured in handwriting samples or in a story completion task in which the patient is required to supply the proper grammatical form of a word that completes a sentence, is not prominent.

The pathophysiology of heroin "overdose" deaths is not fully understood. Surveillance of these deaths and of the heroin content of glassine bags available at the "street level" in Atlanta in the 1971-to-1973 period disclosed a significant correlation between the occurrence of such deaths and the amount of heroin contained in the bags ( P ( JAMA 229:677-678, 1974)

A patient recovering from a severe head injury developed a prolonged Capgras syndrome in which he believed his wife and five children had been replaced by nearly identical substitutes. Although this phenomenon is considered a functional disorder in the psychiatric literature, recent reports postulate an organic basis. Recent studies of the comparable neurologic disorder, reduplicative paramnesia, have stressed the importance of bilateral frontal and right hemisphere pathology. Neuropsychologic and neuroradiologic data in our patient revealed this combination, suggesting that the Capgras syndrome may be a form of reduplicative paramnesia with the same pathologic substrate.

Patients who exhibited frank confabulation were examined with four tests designed to elucidate the nature of confabulation in a structured situation, test the ability of confabulators to use cues, and examine the degree to which certain cognitive deficits are associated with confabulation. Two groups of confabulators emerged: mild and severe. Severity of confabulation was associated with perseveration, impaired self-monitoring facility, and failure to inhibit incorrect responses. Attenuation of these cognitive deficits with resolution of confabulation in a single patient suggested that the two levels of confabulation represented different levels of impairment of the same disorder.

Progressive aphasia without dementia (primary progressive aphasia) is increasingly recognized as an important neurobehavioral syndrome. Clinical diagnosis of progressive aphasia is difficult early in its course, and the differential diagnosis is usually said to include Alzheimer's and Pick's diseases. We report a 61-year-old man with autopsy-proven Creutzfeldt-Jakob disease (CJD) whose major initial manifestation was a progressive, fluent aphasia. Myoclonus was absent, and characteristic EEG abnormalities appeared relatively late. We believe that this case of CJD is unique in its presentation of profound and isolated aphasia. CJD should be considered in the differential diagnosis of the progressive aphasia syndrome.

This text is both easy and difficult to review. It is easy to review because it is a good book: generally well written, very well edited, and comprehensive. It remains disease oriented, as were the previous editions, when the book was the solo enterprise of Dr Merritt. Overall, the editor has been successful in preserving the tone and the voice of Dr Merritt throughout this multiauthored text. Readers of early editions will find this volume familiar. There is, however, variation in the quality of the contribution. I found several sections to be particularly valuable and clearly written— brain edema, tardive dyskinesia, myasthenia gravis, and sleep disorders are some of the areas that were exemplary. I recommend the book to anyone who needs ready access to contemporary information about neurological diseases. In particular, internists, neurosurgeons, physiatrists, and psychiatrists would find this book a useful addition to their libraries. The difficulty in

The function of subcortical nuclear structures in language is uncertain, and language disorders after injury to these structures are described incompletely. We report 15 patients with left putaminal or thalamic hemorrhage, describe the range of language and behavioral disorders produced, and review the potential mechanisms of these disorders. Clinicoanatomic correlations revealed no definite differences between aphasia after hemorrhage in putamen or in thalamus.

We studied a patient with severe on-off phenomena that complicated chronic L-dopa treatment of Parkinson disease. Neuropsychologic testing was performed in both the on and the off states. Compared with the profound changes in motor status, the neuropsychologic alterations were modest: general disinhibition of language, worsened memory, and perseveration.

With increasing frequency, the physician is confronted with the problem of determining the risk of liver toxicity in a person who may have ingested an overdose of acetaminophen. To be effective, antidotal therapy must be given early after acetaminophen ingestion when the patient, despite the toxic injury occurring in his liver, may appear quite well. We have reviewed the cases of the first five persons who came to our institution with a history of having ingested a large overdose of acetaminophen. In each case plasma or serum acetaminophen levels were low and substantial liver injury did not occur. Measurement of acetaminophen levels, indicating the amount of drug absorbed, were a more reliable index of the risk of toxic liver injury and the need for antidotal therapy than the estimate of the dose ingested. ( JAMA 238:500-501, 1977)

• A syndrome of dysarthria following the appearance of small left frontal-lobe lesions has been recognized for many years but identified by numerous labels. Varied terminology has led to confusion in the literature and inadequate recognition of this syndrome as a distinctive clinical entity. We gathered clinical and anatomic (computed tomographic) data on four patients with this dysarthric syndrome and reviewed cases from the literature that contained sufficient clinical and anatomic data for comparison. These patients had a distinctive syndrome of dysarthria without aphasia, caused by small lesions of the motor system for articulation: pars opercularis, inferior prerolandic gyrus, or white matter deep to those regions. This syndrome should be distinguished from Broca's aphasia, Broca's area aphasia, transcortical aphasia, and subcortical aphasia. Aphemia is not mild Broca's aphasia; it is severe dysarthria, at times in the setting of transient Broca's aphasia.

This book is one of a series of color atlases of medicine. With minimal text and 603 illustrations the author attempts to help "senior students" to "understand the significance of [neurologic] signs and their investigation." The author acknowledges the necessity of omissions and "sweeping generalizations" in order to present as much material as possible within the format of this series. He is also limited to topics and diseases that lend themselves to illustration and photography. Given the modest goals and limiting format, it might be expected that the book would focus on common diseases and typical clinical presentations. These prototypical clinical situations could be augmented with schematic illustrations when appropriate, by up-to-date radiological methodology and by gross neuropathology. There are, in fact, several clear and useful lessons that display this optimal use of the book's format: the summary of the aneurysms of the posterior communicating artery and of the cavernous

Analysis of language profiles and CT anatomy in transcortical motor aphasia (TCMA) suggests that the essential lesion is disruption of connections at sites between the supplementary motor area and the frontal perisylvian speech zone. If the lesion is extended, there may also be poor articulation (lesion deep to motor strip for face), impaired auditory comprehension (lesion in anterior head of caudate, anterior limb internal capsule, anterior putamen, and anterior portion of external capsule, claustrum, extreme capsule, and insula), or stuttering (lesion in pars opercularis and lower third of premotor region). This concept unifies disparate anatomic and psychophysiologic observations about three syndromes: classical TCMA, aphasia after left medial frontal infarction, and TCMA during recovery from Broca's aphasia.

Traumatic basal ganglia hemorrhage (TBGH) is probably secondary to rupture of lenticulostriate or anterior choroidal arteries. We evaluated 6 consecutive cases of this entity to define its clinical and pathologic dimensions. Relative frequency of TBGH was 3% (3 left, 3 right) in this acute rehabilitation population. Lesion size and associated pathology varied. Contralateral hemiparesis, present in all, recovered to varying extents, apparently related to lesion location (posterior limb, internal capsule, or midperiventricular white matter), not size. Prolonged muteness occurred in 4 of 6; these 4 patients also had severe diffuse axonal injury. Clinical findings corresponded with previously recognized subcortical hemisphere profiles. All achieved a moderate disability or good recovery rating on the Glasgow Outcome Scale. Rather than any features of the TBGH itself, duration of coma and/or associated temporal herniation predicted slower recovery and worse outcome. In conclusion, TBGH is a rare entity compatible with a favorable recovery, especially when occurring in isolation. The hemorrhage itself determines clinical signs related to particular subcortical structures involved and the side of the lesion. Overall cognitive impairment and speed and quality of recovery are more related to associated cerebral damage.