Rostral Brainstem Research Articles

Age-related physiological responses to emotion anticipation and exposure

Although there is accumulating evidence for physiological and behavioral changes in response to emotion with age, little is known about developmental changes in response to emotion anticipation. Here, we investigated brain activations related to emotion anticipation and exposure, in participants aged between 19 and 54 years. During the anticipation of negative stimuli, a linear decrease of activation with age was detected in the rostral anterior cingulate cortex and brainstem; whereas exposure to negative stimuli revealed decreasing activation in a network of regions implicated in emotion processing and salience detection. The observed results might reflect reduced focusing on negative future events with age, and are in line with an age-related shift of motivational priorities for the pursuit of emotional satisfaction and well being.

PALILALIA IN SIGN LANGUAGE

Sign languages, which use the hands and arms as articulators, are the natural languages of deaf people. Research indicates that sign, like speech, can break down at the level of motor control, in the context of a movement disorder such as Parkinson disease (PD).1 This article describes the first known case of a deaf sign language user with progressive supranuclear palsy (PSP). PSP affects the rostral brainstem and its projections to the basal ganglia, cerebellum, and cerebral cortex.2 Dysarthria typically emerges early in the course of the disease and disrupts several aspects of speech.3 The characteristic features of PSP dysarthria are articulatory incoordination and palilalia—the repetition of entire words at decreasing amplitudes without pause.2 This descriptive case study suggests that those same features are prominent in the sign production of a deaf man with PSP. ### Methods. #### Participants. The individual with PSP was a 79-year-old right-handed man, who was born deaf. He learned British Sign Language (BSL) at school at age 7, and it became his primary language. He developed left-sided weakness and dysphagia at age …

Cortical metabolic changes in the cerebellar variant of multiple system atrophy: A voxel-based FDG-PET study in 41 patients

In addition to neuronal loss in the cerebellum and basal ganglia, recent imaging studies have suggested that cortical involvement may be more extensive in patients with MSA. In this study, we focused on cortical metabolic patterns in 41 patients with MSA-C and 30 controls, using statistical parametric mapping analysis to evaluate whether metabolic derangement in MSA-C patients involved the cortical area and correlated cerebral metabolism with clinical parameters. In patients with MSA-C, SPM analysis revealed that, apart from the expected reduction of FDG-uptake in brainstem–cerebellar area, there was a significant hypometabolism in widespread frontal cortex, including inferior orbitofrontal, rectus, middle and superior frontal, and superior mesiofrontal extending to cingulum, and left inferior parietal cortex. In a subgroup analysis of MSA-C patients, metabolic derangement in the cerebral cortex was visible even in the early stages of MSA-C. In advanced stages, the metabolic derangement tended to evolve into the rostral brainstem and into other cortical areas, including left inferior frontal cortex and right inferior orbitofrontal, right anterior and middle cingulate, and anterior portion of superior mesiofrontal gyri. In correlation analysis, reduced FDG-uptake in orbitofrontal area was most significantly correlated with disease severity and duration, followed by the medial frontal, the dorsal portion of the midbrain, and the cerebellum. Our study demonstrated that there were widespread areas of decreased metabolism in the cerebral cortex and, as the disease progressed, the pattern of metabolic derangement tended to evolve into other frontal areas without significant changes in cerebellar metabolism, suggesting that reduced FDG-uptake in cortical area may be associated with the primary disease process.

Motor Cortex Gates Vibrissal Responses in a Thalamocortical Projection Pathway

Higher-order thalamic nuclei receive input from both the cerebral cortex and prethalamic sensory pathways. However, at rest these nuclei appear silent due to inhibitory input from extrathalamic regions, and it has therefore remained unclear how sensory gating of these nuclei takes place. In the rodent, the ventral division of the zona incerta (ZIv) serves as a relay station within the paralemniscal thalamocortical projection pathway for whisker-driven motor activity. Most, perhaps all, ZIv neurons are GABAergic, and recent studies have shown that these cells participate in a feedforward inhibitory circuit that blocks sensory transmission in the thalamus. The present study provides evidence that the stimulation of the vibrissa motor cortex suppresses vibrissal responses in ZIv via an intra-incertal GABAergic circuit. These results provide support for the proposal that sensory transmission operates via a top-down disinhibitory mechanism that is contingent on motor activity.

Nuclear organization and morphology of serotonergic neurons in the brain of the Nile crocodile, Crocodylus niloticus

The present study describes the location and nuclear organization of the serotonergic system in a representative of the order Crocodylia, the Nile crocodile ( Crocodylus niloticus). We found evidence for serotonergic neurons in three regions of the brain, including the diencephalon, rostral and caudal brainstem, as previously reported in several other species of reptile. Within the diencephalon we found neurons in the periventricular organ of the hypothalamus, but not in the infundibular recess as noted in some other reptilian species. In addition we found serotonergic neurons in the pretectal nucleus, this being the first description of these neurons in any species. Within the rostral brainstem we found medial and lateral divisions of the superior raphe nucleus and a widely dispersed group of neurons in the tegmentum, the superior reticular nucleus. In the caudal brainstem we observed the inferior raphe nucleus and the inferior reticular nucleus. While much of the serotonergic system of the Nile crocodile is similar to that seen in other reptiles the entire suite of features appears to distinguish the crocodile studied from the members of the Squamate (lizards and snakes) and Testudine (turtles, tortoises and terrapins) reptiles previously studied. The observations are suggestive of order-specific patterns of nuclear organization of this system in the reptiles, reflecting potential evolutionary constraints in the mutability of the nuclear organization as seen for similar systems in mammals.

Surgical treatment of ventral mesencephalic cavernoma

The treatment of an intrinsic midbrain tumour has always been controversial due to the precarious nature of its location. We report a rare example of a cavernoma located in the ventral mesencephalon and presented clinically as Holmes' tremor. In order to access this vital portion of midbrain, we chose a fronto-temporal trans-sylvian route via an orbito-zygomatic craniotomy. The cavernoma was removed en bloc with a longitudinal pial incision between the fronto-pontine fibers and the pyramidal tracts in the peduncle. After the operation, the tremor dramatically disappeared. Through a review and analysis of the literature, we discuss the surgical strategy for management of an anterior midbrain cavernoma. With an optimal surgical approach, fairly safe entry zones on the anterior face of the rostral brainstem may be accessible, which makes it possible for successful resection of a ventral mesencephalic cavernoma without postoperative complications.

Auditory brainstem activity and development evoked by apical versus basal cochlear implant electrode stimulation in children

Objective The role of apical versus basal cochlear implant electrode stimulation on central auditory development was examined. We hypothesized that, in children with early onset deafness, auditory development evoked by basal electrode stimulation would differ from that evoked more apically. Methods Responses of the auditory nerve and brainstem, evoked by an apical and a basal implant electrode, were measured over the first year of cochlear implant use in 50 children with early onset severe to profound deafness who used hearing aids prior to implantation. Results Responses at initial stimulation were of larger amplitude and shorter latency when evoked by the apical electrode. No significant effects of residual hearing or age were found on initial response amplitudes or latencies. With implant use, responses evoked by both electrodes showed decreases in wave and interwave latencies reflecting decreased neural conduction time through the brainstem. Apical versus basal differences persisted with implant experience with one exception; eIII–eV interlatency differences decreased with implant use. Conclusions Acute stimulation shows prolongation of basally versus apically evoked auditory nerve and brainstem responses in children with severe to profound deafness. Interwave latencies reflecting neural conduction along the caudal and rostral portions of the brainstem decreased over the first year of implant use. Differences in neural conduction times evoked by apical versus basal electrode stimulation persisted in the caudal but not rostral brainstem. Significance Activity-dependent changes of the auditory brainstem occur in response to both apical and basal cochlear implant electrode stimulation.

Frontal-lobe syndrome and psychosis after damage to the brainstem dopaminergic nuclei

A patient developed frontal-lobe syndrome and psychotic symptoms after infarction in the pontomesencephalic junction. Stereotaxic lesion localization on magnetic resonance imaging and statistical analyses of regional cerebral blood flow (rCBF) disclosed an involvement of the rostral brainstem dopaminergic nuclei and hypoperfusion in the frontal-subcortical circuit components. We suggest that the patient's cognitive and behavioral disturbances were associated with disruption of ascending dopaminergic projections to the frontal-subcortical circuits.

Nociceptive Craniofacial Muscle Primary Afferent Neurons Synapse in Both the Rostral and Caudal Brain Stem

Limited information is available on muscle afferent neurons with fine fibers despite their presumed participation in musculoskeletal disorders, including temporomandibular disorders. To study these neurons, intracellular recordings were made from the central axons of slowly conducting muscle afferent neurons in anesthetized rats. After intraaxonal impalement, axons were characterized by masseter nerve stimulation, receptive field testing, muscle stretching and intramuscular injection of hypertonic saline. Intracellular recordings were made from 310 axons (conduction velocity: 6.5-60(M)/s, mean = 27.3(M)/s; following frequency: 27-250 Hz, mean = 110Hz). No neurons responded to cutaneous palpation or muscle stretching. Some axons (n = 34) were intracellularly stained with biotinamide. These neurons were classified as group II/III noxious mechanoreceptors because their mechanical threshold exceeded 15 mN, and conduction velocities ranged from 12 to 40.2(M)/s (mean = 25.3(M)/s). Two morphological types were recognized by using an object-based, three-dimensional colocalization methodology to locate synapses. One type (IIIHTM(Vp-Vc)) possessed axon collaterals that emerged along the entire main axon and synapsed in the trigeminal principal sensory nucleus and spinal trigeminal subnuclei oralis (Vo), interpolaris (Vi), and caudalis (Vc). A second type (IIIHTM(Vo-Vc)) possessed axon collaterals that synapsed only in caudal Vo, Vi, and Vc. Our previous studies show that muscle spindle afferent neurons are activated by innocuous stimuli and synapse in the rostral and caudal brain stem; here we demonstrate that nociceptive muscle mechanoreceptor afferent axons also synapse in rostral and caudal brain stem regions. Traditional dogma asserts that the most rostral trigeminal sensory complex exclusively processes innocuous somatosensory information, whereas caudal portions receive nociceptive sensory input; the data reported here do not support this paradigm.

Hypothalamic control of sleep

A sleep-promoting function for the rostral hypothalamus was initially inferred from the presence of chronic insomnia following damage to this brain region. Subsequently, it was determined that a unique feature of the preoptic hypothalamus and adjacent basal forebrain is the presence of neurons that are activated during sleep compared to waking. Preoptic area “sleep-active” neurons have been identified by single and multiple-unit recordings and by the presence of the protein product of the c-Fos gene in the neurons of sleeping animals. Sleep-active neurons are located in several subregions of the preoptic area, occurring with high density in the ventrolateral preoptic area (vlPOA) and the median preoptic nucleus (MnPN). Neurons in the vlPOA contain the inhibitory neuromodulator, galanin, and the inhibitory neurotransmitter, GABA. A majority of MnPN neurons activated during sleep contain GABA. Anatomical tracer studies reveal projections from the vlPOA and MnPN to multiple arousal-regulatory systems in the posterior and lateral hypothalamus and the rostral brainstem. Cumulative evidence indicates that preoptic area neurons function to promote sleep onset and sleep maintenance by inhibitory modulation of multiple arousal systems. Recent studies suggest a role for preoptic area neurons in the homeostatic aspects of the regulation of both rapid eye movement (REM) and non-REM (NREM) sleep and as a potential target for endogenous somnongens, such as cytokines and adenosine.

Surgery for mesencephalic cavernoma: case report

Background Intrinsic midbrain tumor has been one of the most challenging therapeutic tasks in neurosurgery because of its prognosis and risks associated with surgical procedures. We encountered a rare case of cavernoma located in the anterior-mesencephalic region presented as parkinsonism tremor. Case Description A 42-year-old woman had a resting tremor for 10 years. This tremor involved the left shoulder and the proximal and distal limb, which was exacerbated by any attempted movement and became grossly uncontrollable. She showed a partial right ophthalmoplegia with mydriasis. Her right upper and lower extremities had normal strength, but her left extremities had three-fifth strength. Her sensation was intact. Magnetic resonance imaging demonstrated a popcorn-like rounded lesion in the right ventral midbrain adjacent to the medial cerebral peduncle. To access this anterior-medial portion of the midbrain, we chose a frontotemporal transsylvian route via an orbitozygomatic craniotomy. With a longitudinal pial incision between the frontopontine fibers and the pyramidal tracts in the peduncle, the cavernoma was totally removed en bloc. After the operation, the tremor dramatically disappeared. The muscle strength of her left lower extremity improved to four fifths, whereas the upper extremity was still the same. The preoperative left oculomotor palsy seemed to have no improvement. Conclusions Clinically manifested cavernoma due to repeated hemorrhage needs surgical intervention. With an optimal surgical approach, fairly safe entry zones on the anterior face of the rostral brainstem may be accessible, which provides a successful resection of a mesencephalic cavernoma without postoperative complications.

Hemodynamic responses and c-Fos changes associated with hypotensive hemorrhage: standardizing a protocol for severe hemorrhage in conscious rats

The central mechanisms underlying the transition from compensation to decompensation during severe hemorrhage (HEM) are poorly understood. Furthermore, a lack of consistency in HEM protocols exists in the current literature. This study assessed the cardiovascular response and Fos-like immunoreactivity (FLI) in specific brain regions following severe HEM at three rates (2, 1, or 0.5 ml.kg(-1).min(-1)) in conscious rats. Heart rate (HR) and arterial pressure were recorded during the withdrawal of 30% of total blood volume (TBV). Data from animals hemorrhaged at the fast (F-HEM, n = 6), intermediate (I-HEM, n = 7), or slow (S-HEM, n = 7) rates were compared with saline (SAL, n = 5) and hypotensive (hydrazaline-induced, HYDRAZ, n = 5) controls. All HEM rates produced similar degrees of hypotension at the time of 30% TBV withdrawal. All HEM rates also produced bradycardia, but the change in HR was only significant in the F-HEM and I-HEM groups. Associated with I-HEM and F-HEM, but not HYDRAZ treatment were significant increases in FLI in the caudal ventrolateral periaqueductal gray (PAG), the central lateral nucleus of the rostral parabrachial nucleus, and locus coeruleus compared with SAL treatment. I-HEM also induced significant increases in FLI in the dorsomedial PAG, A7 region, and the cuneiform nucleus compared with SAL. S-HEM did not induce any significant change in FLI. Our results suggest that HEM at a rate of 1 ml.kg(-1).min(-1) may be most useful for investigating the potential role of the rostral brainstem regions in mediating hemorrhagic decompensation in conscious rats.

Efferent projections of rat rostroventrolateral medulla C1 catecholamine neurons: Implications for the central control of cardiovascular regulation

A replication-defective lentivirus vector that expresses enhanced green fluorescent protein (EGFP) under the control of a synthetic dopamine-beta-hydroxylase (DbetaH) promoter was used to define efferent projections of C1 catecholamine neurons in rat rostral ventrolateral medulla (RVLM). EGFP expression was restricted to C1 neurons and filled their somatodendritic compartments and efferent axons 7-28 days after vector injection. This included the descending projections to thoracic spinal cord and a network in brainstem, midbrain, and diencephalon. In caudal brainstem, restricted terminal fields were present in the dorsal motor vagal complex, A1, raphe pallidus and obscurus, and marginal layer of ventrolateral medulla. Innervation of raphe nuclei was most dense at the level of RVLM, but rostral levels of pallidus were devoid of innervation. A sparse commissural projection to contralateral RVLM was observed, and pericellular arbors were present in the dorsal reticular formation among the projection pathway of catecholamine axons. Rostral brainstem contained a dense innervation of locus coeruleus and the nucleus subcoeruleus. A restricted innervation of the ventrolateral column of the periaqueductal gray distinguished the midbrain. Forebrain labeling was restricted to the diencephalon, where distinctive terminal fields were observed in the paraventricular thalamic nucleus; the lateral hypothalamic area; and the paraventricular, dorsomedial, supraoptic, and median preoptic nuclei of hypothalamus. Projection fibers also coursed through the tuberal hypothalamus into the median eminence. Collectively, these data demonstrate that RVLM C1 neurons modulate the activity of other central cell groups known to participate in the regulation of cardiovascular and autonomic function.

An Evoked Potential Study of the Developmental Time Course of the Auditory Nerve and Brainstem in Children Using Cochlear Implants

Central auditory responses to electrical stimulation from a cochlear implant were studied in 75 pre-lingually deafened children and 11 adults. Electrically evoked auditory brainstem response (EABR) latencies significantly decreased with duration of cochlear implant use and were not significantly affected by the age at implant activation. Significant decreases in early latency waves and interwaves occurred within the first 1–2 months of implant use, whereas longer term changes (6–12 months) were found for eV and eIII-eV, which measure activity in the more rostral brainstem. Comparisons to acoustically evoked auditory brainstem response (ABR) in children with normal hearing suggested shorter interwave EABR latencies, reflecting either distinct neural generators or increased neural synchrony, but similar rates of change in the later latency eV and eIII-eV with time in sound. In sum, normal-like development of the rostral auditory brainstem is promoted by cochlear implant use in children of a wide range of ages.

Nitric Oxide Pathway as New Drug Targets for Refractory Hypertension

Nitric oxide (NO) is thought to reduce blood pressure by evoking vasodilation either directly by causing relaxation of vascular smooth muscle or indirectly by acting in the rostral brainstem to reduce central sympathetic outflow, which decreases the release of norepinephrine from sympathetic nerve terminals. An increasingly large body of literature suggests that alterations in the NO system may play an important role in the development or maintenance of clinical hypertension. As proof of concept, pharmacological inhibition of nitric oxide synthase (NOS) in humans and animals causes moderate to severe hypertension. Certain forms of secondary hypertension are accompanied by the accumulation of endogenous NOS inhibitors, which may contribute to the development of hypertension. Furthermore, targeted disruption of the endothelial isoform of NOS in mice causes moderate hypertension, implying that hypertension may also develop from reductions in NOS expression. These gene knockout studies in animals have initiated the search for single nucleotide polymorphisms in human NOS genes, which could potentially lead to decreases in NOS protein expression. Conversely, increases in NOS expression or NO production have been linked with several commonly used cardiovascular therapies, including exercise training and the use of both statins and angiotensin-converting enzyme inhibitors. Finally, increases in the production of oxidants such as superoxide anion can lead to the inactivation of NO, thereby reducing NO bioavailability. Thus, alterations in the expression or activity of NOS or in the availability of NO have the potential to play a causal role in clinical hypertension. The purpose of this article is to show how emerging basic research on the NO pathway is elucidating novel antihypertensive drug targets that are on the cusp of clinical application.

Encoding of pitch in the human brainstem is sensitive to language experience

Neural processes underlying pitch perception at the level of the cerebral cortex are influenced by language experience. We investigated whether early, pre-attentive stages of pitch processing at the level of the human brainstem may also be influenced by language experience. The human frequency following response (FFR), reflecting sustained phase-locked activity in a population of neural elements, was used to measure activity within the rostral brainstem. FFRs elicited by four Mandarin tones were recorded from native speakers of Mandarin Chinese and English. Pitch strength (reflecting robustness of neural phase-locking at the pitch periods) and accuracy of pitch tracking were extracted from the FFRs using autocorrelation algorithms. These measures revealed that the Chinese group exhibits stronger pitch representation and smoother pitch tracking than the English group. Consistent with the pitch data, FFR spectral data showed that the Chinese group exhibits stronger representation of the second harmonic relative to the English group across all four tones. These results cannot be explained by a temporal pitch encoding scheme which simply extracts the dominant interspike interval. Rather, these results support the possibility of neural plasticity at the brainstem level that is induced by language experience that may be enhancing or priming linguistically relevant features of the speech input.

6.27 A paradigm to assess kinematic responses during anteroposterior translations in sitting following whiplash injuries

Natural soundscapes often contain multiple sound sources at any given time. Numerous studies have reported that in human observers, the perception and identification of concurrent sounds is paralleled by specific changes in cortical event-related potentials (ERPs). Although these studies provide a window into the cerebral mechanisms governing sound segregation, little is known about the subcortical neural architecture and hierarchy of neurocomputations that lead to this robust perceptual process. Using computational modeling, scalp-recorded brainstem/cortical ERPs, and human psychophysics, we demonstrate that a primary cue for sound segregation, i.e., harmonicity, is encoded at the auditory nerve level within tens of milliseconds after the onset of sound and is maintained, largely untransformed, in phase-locked activity of the rostral brainstem. As then indexed by auditory cortical responses, (in)harmonicity is coded in the signature and magnitude of the cortical object-related negativity (ORN) response (150–200 ms). The salience of the resulting percept is then captured in a discrete, categorical-like coding scheme by a late negativity response (N5; ~500 ms latency), just prior to the elicitation of a behavioral judgment. Subcortical activity correlated with cortical evoked responses such that weaker phase-locked brainstem responses (lower neural harmonicity) generated larger ORN amplitude, reflecting the cortical registration of multiple sound objects. Studying multiple brain indices simultaneously helps illuminate the mechanisms and time-course of neural processing underlying concurrent sound segregation and may lead to further development and refinement of physiologically driven models of auditory scene analysis.

See-Saw Nystagmus as the Presenting Sign in Multiple Sclerosis

Although see-saw nystagmus has been reported in multiple sclerosis (MS) (1), there is no previous report of a patient presenting with this finding. A 33-year-old woman reported a 2-day history of oscillopsia. She had no other neurologic or systemic symptoms. On examination, the eyes were aligned with full ductions. The patient had characteristic pendular see-saw nystagmus that increased on left gaze. The velocity of the nystagmus was equal in both directions. The OD ascended and intorted, whereas the OS descended and extorted; then the OD descended and extorted, whereas the OS ascended and intorted. Otherwise, the ophthalmologic and neurologic examination was unremarkable. Total blood count, erythrocyte sedimentation rate, glucose, urea, electrolytes, and a collagen vascular disease profile were normal. Lumbar puncture revealed a normal opening pressure and cerebrospinal fluid formula, but isoelectric focusing showed three positive IgG oligoclonal bands; none was detected from a simultaneous serum sample. Brain magnetic resonance imaging showed a linear area of signal change in white matter adjacent to the body of left lateral ventricle (Fig. 1A) and in the deep white matter of the left frontal lobe (Fig. 1B). The combination of clinical, cerebrospinal fluid, and imaging findings suggested a diagnosis of multiple sclerosis.FIG. 1: A. Axial T2-weighted magnetic resonance imaging shows linear high signal in the white matter adjacent to the body of the left lateral ventricle (arrow). B. Coronal FLAIR magnetic resonance imaging shows high signal in the deep white matter of the left frontal lobe (arrow).The exact mechanism of see-saw nystagmus is still not known. Its frequent association with chiasmal and parasellar lesions initially led to speculation that see-saw nystagmus was related to a disturbance in visual input. Recent evidence suggests that see-saw nystagmus is caused by dysfunction of the rostral brainstem (2). A disturbance in the interstitial nucleus of Cajal, a small collection of neurons located adjacent to medial longitudinal fasciculus in the midbrain tegmentum, is often implicated (2). Soupramanien Sandramouli, FRCS, FRCOphth Hani T. Benamer, MRCP, PhD Mark Mantle, MRCP, FRCR Randhir Chavan, MS Wolverhampton and Midland Counties Eye Infirmary and Departments of Neurology and Radiology; New Cross Hospital; Wolverhampton, England; E-mail: [email protected]

New England medical center posterior circulation stroke registry: I. Methods, data base, distribution of brain lesions, stroke mechanisms, and outcomes.

Among 407 New England Medical Center Posterior Circulation Registry (NEMC-PCR) patients, 59% had strokes without transient ischemic attacks (TIAs), 24% had TIAs before strokes, and 16% had only posterior circulation TIAs. Embolism was the commonest stroke mechanism accounting for 40% of cases (24% cardiac origin, 14% arterial origin, 2% had potential cardiac and arterial sources). In 32%, large artery occlusive lesions caused hemodynamic brain infarction. Stroke mechanisms in the posterior and anterior circulation are very similar. Infarcts most often included the distal posterior circulation territory (rostral brainstem, superior cerebellum and occipital and temporal lobes), while the proximal (medulla and posterior inferior cerebellum) and middle (pons and anterior inferior cerebellum) territories were equally involved. Infarcts that included the distal territory were twice as common as those that included the proximal or middle territories. Most distal territory infarcts were attributable to embolism. Thirty day mortality was low (3.6%). Embolic stroke mechanism, distal territory location, and basilar artery occlusive disease conveyed the worst prognosis.

Blefaroespasmo y blefarocolisis. Caras diferentes de una misma moneda

The eyelid movements are mediated mainly by the orbicularis oculi (OO) and the levator palpebrae superioris (LPS) muscles. Dissociated upper lid functions exhibit different counterbalanced action of these muscles, and in blinking they show a strictly reciprocal innervation. The disturbance of this close LPS-OO relationship likely leads to many of the central lid movement disorders.Two major lid postural disorders, the blepharospasm (BSP) and the blepharocolysis (BCO), share two different clinical aspects: the involuntary eyelids' closure along with the inability to open the eyes. BSP consists of an involuntary overactivity of the OO, with LPS co-contraction activity, and is expressed as frequent and prolonged blinks, clonic bursts, prolonged tonic contraction or a blend of all of them. BCO (commonly named 'so-called lid opening apraxia') is an involuntary overinhibition of the LPS muscles with no evidence of ongoing OO activity; it exists a co-inhibition of these muscles. BSP and BCO occur in many instances of idiopathic dystonias and basal ganglia diseases and, less frequently, in rostral brainstem lesions. Both may coincide in the same patient.BSP and BCO should be considered different expressions of the dystonic focal eyelid movement disorders, related to the increase of the two counteracting components of the normal eyelid motor and blinking patterns: the excessive OO activation in the BSP; the excessive LPS inhibition in the BCO.