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PubMed2003

Multi-unit activity suppression and sensorimotor deficits after endothelin-1-induced middle cerebral artery occlusion in conscious rats.

Conscious Wistar rats with stereotaxically and unilaterally implanted cannula just above the middle cerebral artery (MCA) were injected with the powerful vasoconstrictor peptide endothelin-1 (ET1, 60 pmol in 3 microl). The purpose was to examine the long-term (from the 1st to the 14th day) changes in neuronal bioelectrical activity together with sensorimotor deficits after ET1-induced MCA occlusion (MCAO). Extracellular multi-unit activity (MUA) recorded from the ipsilateral fronto-parietal cortical area (supplied by MCA) and sensorimotor behavior (one postural reflex test and six limb placing tests) were examined. A significant suppression of the multi-unit activity was observed until the 14th day post-ET1. The rats exhibited significant unilateral sensorimotor deficits with a maximum at the 3-7 days after ET1 and a spontaneous partial recovery by days 11-14. A significant correlation was found between the suppression of the multi-unit activity and the sensorimotor deficits between the 3rd and the 10th day post-ET1. The results suggest that studying the bioelectrical activity in combination with the behavioral sensorimotor functions may be of use to assess the functional disturbances associated with focal cerebral ischemia and would help to examine the therapeutic benefits of various cerebroprotective treatments before initiating human clinical trials.

Action Potentials↗
PubMed1997

Comparative assessment of peripheral sympathetic function by postural vasoconstriction arteriolar reflex and sympathetic skin response in NIDDM patients.

PURPOSE: The aim of the study was to compare peripheral sympathetic adrenergic and cholinergic nerve function in NIDDM (non-insulin-dependent diabetes mellitus) patients with various degrees of diabetic neuropathy and neuropathic foot ulceration. The parameters used were postural vasoconstriction arteriolar reflex (VAR) and sympathetic skin response (SSR), respectively. PATIENTS AND METHODS: Forty-seven NIDDM patients were studied. No patients had clinically significant peripheral vascular disease. They were divided according to peripheral somatic neuropathy, assessed by clinical score and vibration perception threshold (VPT). Twenty-two patients showed no significant evidence of peripheral neuropathy and normal VPT (DN-); 15 had signs and symptoms of neuropathy and VPT alteration (DN+); 10 had diabetic neuropathy and foot ulceration (DNU). Twenty-two normal subjects were also examined as a control group. Resting arteriovenous shunt skin blood flow, measured using laser-Doppler flowmetry, and the VAR of the big toe on lowering the foot were studied. Sympathetic skin response was assessed by an EMG apparatus. Autonomic function was also investigated by using standard cardiovascular reflex tests. RESULTS: Resting blood flow values were similar in the three NIDDM groups and in the control group. VAR to foot lowering was significantly impaired in all NIDDM groups by comparison with controls (72.8 +/- 2.1%, mean +/- SEM), this impairment being progressively more pronounced in DN- (58.8 +/- 2.3%, P < 0.001), DN+ (33.3 +/- 3.0%, P < 0.001 versus DN-) and DNU (8.6 +/- 2.7%, P < 0.001 versus DN+). Sympathetic skin response was assessed in 28 patients and was significantly impaired in DN-compared with the control group (2.53 +/- 0.04 versus 2.71 +/- 0.04 log mcV, P < 0.01). This impairment was severe in the DNU compared with the DN+ group (1.36 +/- 0.05 versus 2.26 +/- 0.04 log mcV, P < 0.005). A positive correlation was found between VAR values and SSR (P < 0.001), and these measurements were also closely correlated with several parameters of central autonomic and somatic neuropathy. CONCLUSION: These results indicate that peripheral sympathetic adrenergic and cholinergic fibers simultaneously undergo early alterations in diabetic patients, even when there is no clinical neuropathy. Our data also show almost complete abolition of peripheral sympathetic activity in NIDDM patients with foot ulceration.

Blood Flow Velocity↗
PubMed1994

Subcortical contributions to head movements in macaques. I. Contrasting effects of electrical stimulation of a medial pontomedullary region and the superior colliculus.

1. These studies were initiated to understand the neural sites and mechanisms controlling head movements during gaze shifts. Gaze shifts are made by saccadic eye movements with and without head movements. Sites were stimulated electrically within the brain stem of awake, trained monkeys relatively free to make head movements to study the head-movement components of gaze shifts. 2. Electrical stimulation in and around the gigantocellular reticular nucleus evoked head movements in the ipsilateral direction. Gaze shifts were never evoked from these sites, presumably because the vestibulo-ocular reflex compensated. The rough topography of this region included large head movements laterally, small movements medially, downward movements from dorsal sites, and upward movements more ventrally. 3. The initial position of the head influenced the magnitude of the elicited movement with larger movements produced when the head was directed to the contralateral side. Attentive fixation was associated with larger and faster head movements when compared with those evoked during spontaneous behavior. 4. The superior colliculus makes a significant contribution to gaze shifts and has been shown to contribute to head movements. Because the colliculus is a major source of afferents to the gigantocellular reticular nucleus, comparable stimulation studies of the superior colliculus were conducted. When the colliculus was excited, shifts of gaze in the contralateral direction were predominant. These were most often accomplished by saccadic eye movements, however, we frequently elicited head movements that had an average latency 10 ms longer than those elicited from the reticular head movement region. Sites evoking head movements tended to be deeper and more caudal than loci eliciting eye movements. Neither the onset latencies, amplitudes, nor peak velocities of head movements and eye movements were correlated. Gaze shifts evoked from the caudal colliculus with the head free were larger than those elicited from the same site with the head fixed. 5. These studies demonstrate that both the superior colliculus and gigantocellular reticular nucleus mediate head movements. The colliculus plays a role in orienting to external events, and so collicular head movements predominantly were associated with gaze shifts, with the eye and head movements uncoupled. The medullary reticular system may play a role in the integration of a wider range of movements. Head movements from the medullary reticular sites probably participate in several forms of head movements, such as those that are related to postural reflexes, started volitionally, and/or oriented to external events.

Animals↗
PubMed2000

An autopsy case of autosomal-recessive juvenile parkinsonism with a homozygous exon 4 deletion in the parkin gene.

We report the neuropathologic and genetic features of a 70-year-old man with autosomal-recessive juvenile parkinsonism (AR-JP). At the age of 32 years, he developed a dystonic gait, followed by hand tremor, rigidity, bradykinesia, and impaired postural reflex. Levodopa was effective in ameliorating these symptoms. Pathologic examination of autopsy specimens from this patient revealed loss of pigmented neurons and gliosis in the substantia nigra pars compacta (SNPC), being most pronounced in the medial and ventrolateral regions, and locus ceruleus (LC). The melanin content of the remaining SNPC neurons was low. This feature was less marked in the LC. There were no Lewy bodies, as confirmed by immunostaining for alpha-synuclein. An additional, significant finding in this patient was neuronal loss and fibrillary gliosis in the substantia nigra pars reticulata; this feature has not been reported previously in AR-JP. Gene analysis revealed that this autopsied patient and his siblings had the parkin gene mutation (homozygous exon 4 deletion) that is responsible for the disease.

Aged↗
PubMed1997

Familial parkinsonism, dementia, and Lewy body disease: study of family G.

Genetic influences are thought by many to play an important role in the cause of Parkinson's disease. We studied two closely intermarried families (Family G) whose ancestors immigrated to the United States from Russia. We investigated this family clinically, genealogically, and pathologically. Our pedigree contained 102 members spanning six generations, with 10 affected individuals and 1 affected spouse. Detailed telephone interviews were conducted with affected individuals, with their spouses, and with their at-risk siblings. Medical records of deceased and living affected patients were collected. Physical examinations were performed on 7 at-risk and 5 affected persons. Typical levodopa-responsive parkinsonism with bradykinesia, rigidity, resting tremor, and impaired postural reflexes was seen in 4 members, dementia was present in 3, and 3 had both dementia and parkinsonism. An autopsy completed on 1 individual, our index case, demonstrated Lewy bodies in the brainstem and neocortex and ubiquitin-positive neuritic degeneration in the CA2-3 region of the hippocampus, consistent with the limbic (transitional) form of Lewy body disease. This family is distinct both clinically and pathologically from several previously reported parkinsonian kindreds.

Aged↗
PubMed2002

Dopa-responsive parkinsonism secondary to right temporal lobe haemorrahage.

A 46-year-old man developed a symmetrical parkinsonian syndrome 7 weeks after large right temporal intracerebral haemorrhage resulting from a ruptured arteriovenous malformation. His signs included bradykinesia, rigidity, start hesitation, and poor postural reflexes, without a resting tremor. He also had signs of a Parinaud's syndrome. Computed tomography and magnetic resonance imaging of the brain demonstrated changes in the right temporal lobe associated with the haemorrhage but no abnormality of the basal ganglia or midbrain. Levodopa therapy produced a dramatic improvement within a few days of commencement. We postulate that the parkinsonism resulted from midbrain compression secondary to transtentorial herniation. Although parkinsonism is a rare complication of lobar intracerebral haemorrhage, it is important to recognise as it may be potentially treatable.

Antiparkinson Agents↗
PubMed2002

Pathophysiology of Parkinson's disease: from clinical neurology to basic neuroscience and back.

Parkinson's disease (PD) is characterized by motor and nonmotor (cognitive and limbic) deficits. The motor signs of PD include hypokinetic signs such as akinesia/bradykinesia, rigidity and loss of normal postural reflexes, and hyperkinetic signs such as tremor. Dopamine depletion in the striatum is the hallmark of PD and of its animal models, still the pathophysiology of the parkinsonian symptoms and especially of parkinsonian tremor are under debate. The most extreme hypotheses argue about peripheral versus central nervous system origin, intrinsic cellular oscillator versus network oscillators, and basal ganglia-based pathophysiology versus cerebellar-thalamic based pathophysiology. Recent studies support the view that parkinsonian symptoms are most likely due to abnormal synchronous oscillating neuronal activity within the basal ganglia. Peripheral factors do only play a minor role for the generation, maintenance, and modulation of PD tremor and other signs. The most likely candidates producing these neuronal oscillations are the weakly coupled neural networks of the basal ganglia-thalamo-cortical loops. However, the present evidence supports the view that the basal ganglia loops are influenced by other neuronal structures and systems and that the tuning of these loops by cerebello-thalamic mechanisms and by other modulator neurotransmitter systems entrain the abnormal synchronized oscillations. Neurosurgical procedures, such as lesions or high-frequency stimulation of different parts of the loop, might resume the normal unsynchronized activity of the basal ganglia circuitry, and, therefore, ameliorate the clinical symptoms of Parkinson's disease.

Animals↗
PubMed2003

Chemotherapy-induced parkinsonism responsive to levodopa: an underrecognized entity.

Parkinsonism is a rare neurological complication of cancer treatment. Although individual case reports of this syndrome have been reported, the clinical features and prevalence of this syndrome are unknown. We present 3 patients, encountered over 6 months at one institution, who developed parkinsonism after treatment with various chemotherapeutic agents. Parkinsonism was severe in 2 patients, affecting postural reflexes, speech, and swallowing. All 3 patients responded dramatically to treatment with levodopa, and parkinsonism spontaneously improved or remitted over months. This unusual complication of cancer therapy is treatable and may be underappreciated.

Aged↗
PubMed2007

Vitamin D and Parkinson's disease--a hypothesis.

Parkinson's disease (PD), a common disease of the elderly, is a movement disorder characterized by tremor, akinesia, and loss of postural reflexes, leading to immobility and frequent falls. It results from selective loss (death) of dopaminergic neurons in the substantia nigra region of the brain, largely developed prior to clinical diagnosis, and continuous after diagnosis, despite use of current therapeutic modalities. In PD in the United States the cause and mechanism of continued neuron cell death in the substantia nigra is currently unknown. We hypothesize, based upon several lines of evidence, that documented chronically inadequate vitamin D intake in the United States, particularly in the northern states and particularly in the elderly, is a significant factor in the pathogenesis of PD. This hypothesis implies that dietary aid for prevention and therapy for PD is possible.

Calcitriol↗
PubMed1997

Cerebellar presentation of multiple system atrophy.

Early diagnosis of multiple-system atrophy (MSA) is important in patients presenting with late-onset cerebellar ataxia because it has a less favourable prognosis than other degenerative ataxic disorders. We report cerebellar presentation of MSA in a series of 16 patients, 3 of whom later developed parkinsonism. Two-thirds of them had early evidence of impaired postural reflexes with a history of recurrent falls. Some of these had a narrow-based, unsteady gait, unlike the more classic broad-based gait ataxia of cerebellar disease. On review of the patients' histories, genitourinary dysfunction (particularly impotence) was present at the onset of, or preceding, cerebellar ataxia in 60% of patients, but this had often been attributed to age, or to urological or gynaecological causes. External striated anal or urethral sphincter electromyography (EMG) demonstrated features of chronic denervation and reinnervation in 14 (93%) of 15 patients, consistent with degeneration in Onuf's nucleus as occurs in MSA. Autonomic function tests were abnormal in 9 (64%) of 14 patients. Our data suggest that close enquiry into genitourinary function and analysis of the gait disorder can be useful pointers to a diagnosis of MSA in patients with an unexplained adult-onset progressive cerebellar syndrome, and that sphincter EMG is the most useful investigation in this context.

Adult↗
PubMed1998

Young-onset Parkinson's disease revisited--clinical features, natural history, and mortality.

The authors report on clinical features and mortality rates in a group of 149 patients with apparent idiopathic parkinsonism starting before the age of 40 years. Ten had juvenile parkinsonism (JP; onset before age 21 years) and 139 had young-onset Parkinson's disease (YOPD; onset at age 21 to 40 years). Included were 60 patients originally reported 10 years ago. Fifty percent of the JP group had a positive family history of parkinsonism in a first-degree relative, and clinical presentation was heterogeneous. Mortality risk was threefold that of the normal population. In the YOPD group, the mortality risk was double that of the normal population. Poor initial response to L-dopa was a risk factor for early death. In two previously reported patients, the diagnosis had been changed to multiple system atrophy and Machado-Joseph disease. After a median disease duration of 18 years, cognitive impairment was found in only 19% of YOPD patients (13% of those younger than 60 years and 43% of those 60 years or older). Age was the most important factor for development of dementia, but female sex and positive family history of parkinsonism also had more modest predictive value. After a disease duration of 10 years or less, only 5% of patients were experiencing falls and 30% freezing, but all patients had developed L-dopa-related fluctuations and dyskinesias. The authors conclude that the mortality rate in parkinsonism starting before the age of 40 is increased in comparison to the normal population and is similar to the general Parkinson's disease population. Intellectual function and postural reflexes are usually well preserved for many years despite a long history of parkinsonism and the early and frequent occurrence of treatment complications, provided the patients remain biologically and chronologically young.

Adolescent↗
PubMed1994

Behavioral specializations of SI and SII cortex: a comparative examination of the neural logic of touch in rats, cats, and other mammals.

In what ways do passive touch and active touch require particular properties of cortical physiology? Because it is not easy to make predictions "bottom up" from neurophysiology and anatomy to behavior, there have been surprises in studying behavioral deficits following selective ablations of SI versus SII. For example, in earlier research on cats, unilateral ablation of SI unexpectedly had no effect on passive touch but did cause contralateral losses in posture and movement; it was ablation of SII plus subjacent cortex that led to contralateral losses in passive touch. In contrast, in a recent experiment with rats unilateral ablation of either SI or SII caused contralateral losses both in touch and postural reflexes. Some of the literature on dogs, monkeys, and humans suggests similarities with cats. To better understand these comparative findings, the following theoretical factors are considered: the degree of diffuseness versus specificity in brain input-output relations demanded or permitted by a behavior, the spatial and temporal scales of a behavior, the species' degree of encephalization, the need for stimulus generalization or functional equivalence of movements, and the relative sizes and sensitivities of different parts of the body. Hypotheses are also offered about why the evolution in rats of shortened forelimbs and increased vibrissal function may have entailed a peculiar compromise between active and passive touch and between functions of SI and SII.

Animals↗
PubMed1997

Delayed antagonism of AMPA/kainate receptors reduces long-term functional deficits resulting from spinal cord trauma.

Excitatory amino acid (EAA) receptors play a significant role in delayed neuronal death after ischemic and traumatic injury to the CNS. Focal microinjection experiments have demonstrated that 2,3-dihydro-6-nitro-7-sulfamoyl-benzo(f)quinoxaline (NBQX), a highly selective and potent antagonist of non-N-methyl-D-aspartate ionotropic EAA receptors, i.e., those preferring alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) or kainate, can reduce histopathology and functional deficits when administered at 15 min after traumatic spinal cord injury (SCI). Similarly, intravenous infusion of NBQX, beginning at 15 min postinjury (p.i.), results in a significant amelioration of the functional deficits produced by experimental SCI. However, if antagonists of AMPA/kainate receptors were to be used therapeutically for patients with SCI, administration would likely be delayed for several hours after injury. We therefore examined the effects of NBQX administered at 4 h after SCI on functional deficits and histopathology in a standardized rat model of contusive SCI. An incomplete SCI was produced in Sprague-Dawley rats at T8 with a weight-drop device (10 g x 2.5 cm). NBQX (15 nmol), or vehicle alone, was microinjected into the injury site 4 h later. Recovery of hind limb reflexes, postural control, and locomotor function was determined by a battery of behavioral tests performed for 8 weeks. Spinal cord tissue was then fixed by perfusion and used for morphometric and immunocytochemical analyses. Previous studies with acute NBQX treatment showed significant functional improvement by 1 week; the effects of delayed NBQX treatment on functional deficits were not discernible until 3-4 weeks after SCI. Thereafter, significant reductions in hindlimb deficits were demonstrated in two independent studies. The nature and magnitude of the reductions in chronic deficits were similar to those observed previously when NBQX was administered acutely at 15 min after SCI. Morphometric analyses showed that delayed treatment with NBQX resulted in sparing of gray matter adjacent to the injury site but no significant effect on the area of white matter at the epicenter. However, serotonin immunoreactivity below the lesion, used as a marker for preservation of one supraspinal pathway, was significantly higher in the NBQX-treated group. These results support a therapeutic potential for NBQX, and presumably other AMPA antagonists, in SCI by demonstrating effectiveness in a clinically relevant time frame. They indicate the importance of assessing chronic functional deficits in evaluating the therapeutic potential of a treatment paradigm. Further, they suggest the intriguing hypothesis that mechanisms underlying early functional recovery after SCI are, at least in part, distinct those from those involved in reducing chronic functional deficits.

Animals↗
PubMed2001

Effect of FK-506 on inflammation and behavioral outcome following intracerebral hemorrhage in rat.

Beginning 15 min after induction of intracerebral hemorrhage (ICH) by intrastriatal administration of collagenase, rats were treated intramuscularly with FK-506 (3 mg/kg) or with vehicle. Treatment was repeated daily for 7 days. MR imaging 1, 7, and 28 days post-ICH showed that treatment did not affect hematoma size or its subsequent resolution. Two days post-ICH, neutrophil infiltration around the hematoma was decreased in the FK-506-treated rats, as was the number of TUNEL-positive cells at the edge of the hematoma and in the peripheral region. The decreased inflammatory response was accompanied by functional improvement in the treated rats. The neurological deficit induced by the ICH (beam walking ability, postural reflex, spontaneous circling) was significantly decreased from 3 to 21 days post-ICH by treatment with FK-506. Skilled use of the forelimb ipsilateral to the ICH was improved and sensory neglect of the same limb was decreased 8-9 weeks post-ICH in rats treated with FK-506. However, neuronal loss assessed 9 weeks post-ICH was not different in the treated and untreated rats.

Animals↗
PubMed1991

Sensitivity of external cuneate neurons to neck rotation in three-dimensional space.

A functionally meaningful vestibular-neck interaction, such as it has been demonstrated for postural reflexes and self-motion perception, requires the spatial and temporal response characteristics of vestibular and neck signals to be similar. We investigated the spatial coding in neurons of the external cuneate nucleus (ECN) with natural neck and vestibular stimulations, and compared them to that of neurons in the descending and medial vestibular nuclei (DVN and MVN, respectively) obtained with vestibular stimulation. Neurons were recorded extracellularly in chronically prepared cats held under light barbiturate anesthesia. Neck stimulation was performed by sinusoidally rotating the animals' trunk relative to the earth-fixed head in six different vertical planes and in the horizontal plane. Vestibular stimulation was elicited by whole-body rotations in the corresponding planes. During neck stimulation in the vertical planes, most ECN neurons showed an approximately sinusoidal discharge modulation about resting rate, which became maximal during rotation in a specific plane. Off this plane, the response declined along a cosine function and reached zero in the orthogonal plane. The majority of these ECN neurons also responded to horizontal neck rotation; the resulting "optimal" direction of rotation in three-dimensional space varied considerably among the neurons. Yet, there was a certain preference; the majority of these ECN neurons fired maximally if trunk rotation in the yaw plane stretched the neck on the ipsilateral side, if roll brought the contralateral shoulder closer to the head, and if pitch brought the back closer to the occiput. A minority of ECN neurons showed more complex response patterns which could not be described by a single, optimal direction. About one third of the neck-sensitive ECN neurons tested showed weak responses during whole body rotation, which might stem from a weak vestibular input to this nucleus. In the DVN and MVN, the optimal direction in three-dimensional space with vestibular stimulation typically had a cosine-like spatial tuning. The spatial distribution of these directions clearly differed from that of neck-sensitive neurons in the ECN. We therefore assume that a further processing of the two input signals takes place at later stages in the CNS (e.g., in the vestibulo-cerebellum) in order to yield a functionally useful vestibular-neck interaction.

Animals↗
PubMed1985

Canal-neck interaction in vestibular neurons of the cat's cerebral cortex.

Interaction of semicircular canal and neck proprioceptive inputs was studied in the cerebral cortex of awake, intact cats. Neuronal responses were recorded extracellularly in the anterior suprasylvian gyrus of the left hemisphere. Stimulations consisted of horizontal rotations in the dark applied as sinusoids or position ramps. There were three stimulus conditions: (1) Pure canal stimulation; rotation of whole body. (2) Pure neck stimulation; rotation of trunk about stationary head. (3) Canal-neck interaction; rotation of head about stationary trunk. We recorded 105 neurons with either Type I or Type II canal response. These showed often pronounced non-linearities such as a clear firing increase upon rotation in the "on-direction" and hardly any decrease in the opposite direction. The responses reflected mostly angular velocity, but angular position signals were also obtained. In 79 neurons, either Type I or Type II neck responses were obtained. They coded either angular velocity, velocity plus position, or position. Canal-neck convergence was found in 67 of 88 neurons tested. In the majority of neurons, interaction was "antagonistic" in the sense that the canal and neck responses tended to cancel each other during rotation of the head about the stationary trunk. These neurons could signal trunk rotation in space rather than head in space or head relative to trunk. Most of the remaining neurons showed a "synergistic" interaction such that the response upon head rotation was enhanced as compared to whole body or trunk rotation. These neurons might be involved in the dual task of monitoring head rotation in space and relative to trunk. Interaction was compatible with linear summation of canal and neck inputs in 70% of the neurons. In part of these, however, the assumption had to be made that the interaction had taken place already at some stage prior to the cortical neurons investigated. The response characteristics of cortical canal neurons are discussed in comparison to vestibular nuclear neurons. Furthermore, parallels are drawn between the observed canal-neck interactions in the cortical neurons and (i) interactions of canal and neck dependent postural reflexes in the decerebrate cat, and (ii) interactions of canal and neck induced turning sensations in man.

Animals↗
PubMed1983

The role of canal-neck interaction for the perception of horizontal trunk and head rotation.

The present report considers the conscious perception of passive horizontal rotations of the trunk, the head, or both, by human observers. It examines in particular how this perception depends on the interaction of canal and neck afferents. Three sets of sinusoidal stimulations (0.2 Hz) were applied to subjects (Ss): Rotations of (1) whole body (pure labyrinthine stimuli, lambda), of (2) only the trunk with the head stationary in space (pure neck stimuli, nu), and of (3) both head and trunk, each with an amplitude and a direction of its own, giving rise to various in-phase and counter phase combinations of lambda and nu.--The Ss were to estimate the magnitude of their turning sensations (psi). In doing so, they were to concentrate either on the rotation of their trunk in space (TS) or of their head in space (HS), or of the head relative to the trunk (HT). The TS and HS turning sensations induced by pure lambda-stimuli were essentially the same as to magnitude and direction. Pure nu-stimulation also led to TS and HS turning sensations. However, the former had the direction of the trunk-to-head (T delta S) deflection, the latter that of the head-to-trunk deflection. The nu-induced HS turning sensation represented an illusion, since the head remained stationary in space. When the lambda- and nu-stimuli were combined, the interaction could be described by a linear summation of their effects. The estimates of TS turning followed the equation psi HS approximately lambda-nu, thus well reflecting the actual TS rotation. The estimates of HS could be described by psi HS approximately lambda+k nu; the term k nu represents the "nu-illusion" contaminating the HS turning sensation. The estimates of HT turning were roughly proportional to nu alone and, therefore, close to the actual HT rotation. We conclude that humans may derive a rather faithful information about trunk rotation from the combined activation of canal and neck afferents, but that the sensation of passive head rotation is contaminated by an (illusionary) contribution from neck afferents. These additive and subtractive modes of interaction have parallels in postural reflexes as well as in neuronal responses that are known from cat.

Adolescent↗