Body Lateropulsion in Stroke: Case Report and Systematic Review of Stroke Topography and Outcome.

INTRODUCTION: Body lateropulsion (BLP) is seen in neurological lesions involving the pathways responsible for body position and verticality. We report a case of isolated body lateropulsion (iBLP) as the presentation of lateral medullary infarction and conducted a systematic literature review. METHODS: MEDLINE and EMBASE databases were searched up to December 3, 2020. INCLUSION CRITERIA: age ≥ 18, presence of BLP, confirmed stroke on imaging. EXCLUSION CRITERIA: age < 18, qualitative reviews, studies with inadequate patient data. Statistical analysis was performed using IBM® SPSS® Statistics 20. RESULTS: A 64-year-old man presented with acute-onset iBLP. Brain MRI demonstrated acute infarction in the right caudolateral medulla. His symptoms progressed with ipsilateral Horner syndrome over the next 24 hours and contralateral hemisensory loss 10 days later. Repeat MRI showed an increase in infarct size. BLP resolved partially at discharge. Systematic review: 418 abstracts were screened; 59 studies were selected reporting 103 patients. Thirty-three patients had iBLP (32%). BLP was ipsilateral to stroke in 70 (68%) and contralateral in 32 (32%). The most common stroke locations were medulla (n = 63, 59%), pons (n = 16, 15%), and cerebellum (n = 16, 15%). Four strokes were cortical, 3 frontal and 1 temporoparietal (3%). The most common etiology was large-artery atherosclerosis (LAA) in 20 patients (32%), followed by small-vessel occlusion in 12 (19%). Seventeen (27%) had large-vessel occlusion (LVO), 12 involving the vertebral artery. Sixty (98%) had some degree of resolution of BLP; complete in 41 (70%). Median time-to-resolution was 14 days (IQR 10-21). There was no relationship between time-to-resolution and age, sex, side of BLP or side of stroke. CONCLUSION: BLP was commonly seen with medullary infarction and was the isolated finding in one-third. LAA and LVO were the most common etiologies. Recovery of BLP was early and complete in most cases.

Neuroanatomical basis of Wallenberg syndrome.

Wallenberg syndrome, or lateral medullar syndrome, is the clinical presentation of the infarct in the territory of posterior inferior cerebellar artery. Its signs and symptoms include vertigo, nystagmus, diplopia, ipsilateral Horner syndrome, facial ruddiness and dry skin, dysphonia, dysphagia, dysarthria, ipsilateral loss of gag reflex, ipsilateral ataxia, ipsilateral impaired taste, ipsilateral facial pain and paresthesia, decreased ipsilateral blink reflex, contralateral hypoalgesia and thermoanaesthesia in the trunk and limbs; and ipsilateral facial hypoalgesia and thermoanaesthesia. Neuroanatomical knowledge is essential to its comprehension, study and diagnosis, because the classic neurological manifestations are easy to explain and understand if function and localization of affected anatomical structures are known as if the posterior cerebral circulation is.

El síndrome de Wallenberg, o síndrome bulbar lateral, es la manifestación clínica del infarto en el territorio de irrigación de la arteria cerebelosa posteroinferior. Su presentación incluye vértigo, nistagmo, diplopía, síndrome de Horner, rubicundez y anhidrosis facial homolateral, disfonía, disfagia, disartria, pérdida homolateral del reflejo nauseoso, ataxia homolateral, disgeusia homolateral, dolor y parestesia faciales homolaterales, pérdida o disminución homolateral del reflejo corneal, hipoalgesia y termoanestesia de tronco y extremidades contralaterales, hipoalgesia y termoanestesia facial homolateral. El conocimiento neuroanatómico es imprescindible para su comprensión, estudio y diagnóstico, ya que sus manifestaciones neurológicas clásicas son fácilmente explicables y entendibles si se conocen la función y la localización de las estructuras anatómicas afectadas, así como la irrigación cerebral posterior.

Investigation of Pupillary Changes After Carotid Endarterectomy and Carotid Stent Placement Using Automated Pupillometry.

INTRODUCTION: Horner's syndrome has been reported after carotid artery endarterectomy (CEA) and carotid artery stenting (CS). This study evaluates pupillary changes after these procedures using automated pupillometry. METHODS: Retrospective analysis from a prospective database of pupillometry readings. Cases (14 patients with CEA/CS) were matched to controls (14 patients without CEA/CS). t test models were constructed to examine pupillary light reflex measures for CEA, CS, and controls. RESULTS: The 28 subjects had a mean age of 70 years, 50% were male, and 96% were Caucasian. There was no significant difference in the mean pupil size, constriction velocity (CV), dilation velocity (DV) between the procedural side compared to the contralateral side. However, the mean DV in the left eye after a left sided procedure among CS patients (.67) was lower than mean DV in left eye among controls (.88; P < .0001) and patients undergoing CEA (1.03; P < .0001). DISCUSSION: CS may result in disruption of the carotid artery plexus and decreased sympathetic response thereby reducing DV in the ipsilateral pupil. In addition, decreased CV can also been seen. CONCLUSION: The findings confirm and extend those of previous authors suggesting that pupillary changes may be seen after CS and automated handheld pupillometry may aid in the detection of Horner Syndrome.

Harlequin Syndrome in Acute Thalamic Hemorrhage.

Harlequin syndrome is a disorder of the autonomic nervous system. It clinically presents as a distinct line of hemifacial sympathetic denervation. We describe a case of Harlequin syndrome with co-existing central first-order Horner syndrome in the setting of a large thalamic hemorrhage with intraventricular extension.

Transient iatrogenic Horner's syndrome following carotid endarterectomy.

We present a case of a 72-year-old man who developed a transient Horner's syndrome in the immediate postoperative period after right carotid endarterectomy which resolved within 3 months. Although Horner's syndrome has been reported with several disorders of the carotid artery, our case documents a rare iatrogenic oculosympathetic paresis after elective carotid endarterectomy.

Twenty-Four Syndrome: An Untold Presentation of Pontine Hemorrhage.

Pontine hemorrhages are relatively uncommon. Various atypical manifestations of pontine stroke like eight-and-a-half syndrome, fifteen-and-a-half syndrome, and sixteen syndrome have been described in the past. We came across a case of pontine bleed that presented with bilateral facial palsy, bilateral horizontal gaze palsy, and contralateral sensorineural hearing loss accounting to the hitherto not described "twenty-four syndrome" with Horner's syndrome and left hemiparesis.

Horner Syndrome: A Clinical Review.

Horner syndrome results from an interruption of the oculosympathetic pathway. Patients with Horner syndrome present with a slightly droopy upper lid and a smaller pupil on the affected side; less commonly, there is a deficiency of sweating over the brow or face on the affected side. This condition does not usually cause vision problems or other significant symptoms, but is important as a warning sign that the oculosympathetic pathway has been interrupted, potentially with serious and even life-threatening processes. The oculosympathetic pathway has a long and circuitous course, beginning in the brain and traveling down the spinal cord to exit in the chest, then up the neck and into the orbit. Therefore, this syndrome with unimpressive clinical findings and insignificant symptoms may be a sign of serious pathology in the head, chest, or neck. This clinical review discusses how to identify the signs, confirm the diagnosis, and evaluate the many causes of Horner syndrome.

Efficacy of digital pupillometry for diagnosis of Horner syndrome.

OBJECTIVES: To evaluate the efficacy of digital pupillometry in the diagnosis of anisocoria related to Horner syndrome in adult patients. DESIGN: Retrospective, observational, case control study. METHODS: Nineteen patients with unilateral Horner syndrome (Horner group) and age-matched controls of 30 healthy individuals with normal vision and neither optic nerve dysfunction nor pupillary abnormalities were included. Pupillary light reflex (PLR) of the Horner group and controls were measured by a dynamic pupillometer (PLR-200; NeurOptics Inc., Irvine, USA). Minimal and maximal (min/max) pupil diameters, latency, constriction ratio, constriction velocity, dilation velocity, and total time taken by the pupil to recover 75% of maximal pupil diameter (T75) were noted. PLR were measured at baseline in both groups and at 30-45 minutes later after 0.5% apraclonidine (Iopidine®; Alcon Laboratories, Fort Worth, TX, USA) instillation in the Horner group. MAIN OUTCOME MEASURES: The PLR parameters in the affected eye and inter-eye difference before and after 0.5% apraclonidine instillation. RESULTS: In the Horner group, pupil diameters and T75 showed significant difference between the affected eye and unaffected contralateral eye at baseline (all P<0.00625). Compared to controls, inter-eye difference values of pupil diameters and T75 were significantly larger in the Horner group (all P<0.001). After 0.5% apraclonidine instillation, changes in pupil diameter and constriction ratio were significantly larger in the affected eye compared to the unaffected contralateral eye (all P<0.00625). The area under the receiver operating characteristic curves for diagnosing Horner syndrome were largest for baseline inter-eye difference in min/max pupil sizes (AUC = 0.975, 0.994), T75 (AUC = 0.838), and change in min/max pupil sizes after apraclonidine instillation (AUC = 0.923, 0.929, respectively). The diagnostic criteria for Horner syndrome relying on baseline pupillary measurements was defined as one of the two major findings; 1) smaller maximal pupil diameter in the affected eye with an inter-eye difference of > 0.5 mm, or 2) T75 > 2.61 seconds in the affected eye, which showed a sensitivity of 94.7% and specificity of 93.3%. The diagnostic accuracy of apraclonidine testing showed a sensitivity of 84.6% and specificity of 92.3%. CONCLUSIONS: Digital pupillometry is an objective method for quantifying PLR. Baseline inter-eye difference in maximal pupil sizes and dilation lag measured by T75 was equally effective in the diagnosis of Horner syndrome compared to the reversal of anisocoria after apraclonidine instillation.

Harlequin sign concomitant with Horner syndrome after anterior cervical discectomy: a case of intrusion into the cervical sympathetic system.

Harlequin syndrome is a rare autonomic disorder referring to the sudden development of flushing and sweating limited to one side of the face. Like Horner syndrome, associating miosis, ptosis, and anhidrosis, Harlequin syndrome is caused by disruption of the cervical sympathetic pathways. Authors of this report describe the case of a 55-year-old female who presented with both Harlequin sign and Horner syndrome immediately after anterior cervical discectomy (C6-7) with cage fusion and anterior spondylodesis. They discuss the pathophysiology underlying this striking phenomenon and the benign course of this condition. Familiarity with this unusual complication should be of particular interest for every specialist involved in cervical and thoracic surgery.

The Degree of Anisocoria in Pediatric Patients With Horner Syndrome When Compared to Children Without Disease.

PURPOSE: To study the magnitude of anisocoria in pediatric patients using the plusoptiX A08 (plusoptiX GmbH, Nuremberg, Germany) photoscreener as compared to a literature review of pediatric patients with known Horner syndrome to determine if anisocoria alone should raise suspicion for the diagnosis. METHODS: The medical records of 592 consecutive patients, neonates to 9 years old, were collected and analyzed. All patients had complete ophthalmic examinations that included photoscreening with the plusoptiX A08. Data included age, pupil sizes, and anisocoria. A complete literature search of documented pupillary size in pediatric patients with the diagnosis of Horner syndrome was performed. This was then compared to the normative pediatric pupil data from the study. RESULTS: Of the 592 children without Horner syndrome, 372 had an anisocoria of 0.1 to 0.5 mm (62.84%), 167 had an anisocoria of 0.6 to 1.2 mm (28.16%), and 21 had an anisocoria of 1.3 mm or greater (3.70%). There was no correlation between increasing age and severity of anisocoria (P = .55). For pediatric patients with a diagnosis of Horner syndrome, the average level of anisocoria was 1.37 mm in room light and 2 mm in darkness. In room light, three children had anisocoria of 0.1 to 0.5 mm (9.4%), 14 had anisocoria of 0.6 to 1.2 mm (43.8%), and 15 had anisocoria of 1.3 mm or greater (46.9%). In darkness, the level of anisocoria increased in 19 patients, causing the first category, 0.1 to 0.5 mm, to include 1 patient (3.1%), the second group to include 5 patients (15.6%), and the last group to include 26 patients (81.3%). Other associated signs/symptoms included ptosis (100%), heterochromia (28.1%), anhidrosis (9.4%), straight hair on affected/curly on unaffected side (9.4%), and neck mass (6.3%). In 37.5% of cases, imaging results were negative and no specific etiology was determined. CONCLUSIONS: In a study of 592 children without Horner syndrome, the average pupillary size increased with age, but the degree of anisocoria remained stable with increasing age. Over half of the children studied had anisocoria up to 0.5 mm (62.84%), but rarely had anisocoria greater than 1.3 mm (3.70%). In children with a diagnosis of Horner syndrome, the majority had anisocoria greater than 1.3 mm, with the discrepancy in pupil size becoming more apparent in low levels of light intensity. Anisocoria greater than 1.3 mm is unlikely to be physiologic in a child; therefore, he or she should be carefully evaluated for other localizing signs, such as ptosis, anhidrosis, and neck mass. [J Pediatr Ophthalmol Strabismus. 2016;53(3):186-189.].

Horner's Syndrome after Scalene Block and Carotid Dissection.

BACKGROUND: Horner's syndrome refers to the clinical triad of ptosis, miosis, and anhidrosis resulting from disruption of the ocular and facial sympathetic pathways. A myriad of etiologies can lead to Horner's syndrome; awareness of the underlying anatomy can assist physicians in identifying potential causes and initiating appropriate care. CASE REPORT: Two patients presented to our Nashville-area hospital in 2014. Patient 1 was a 26-year-old man who noticed facial asymmetry one day after an outpatient orthopedic procedure. His symptoms were attributed to his posterior interscalene anesthesia device; with deactivation of this device, the symptoms rapidly resolved. Patient 2 was a 42-year-old man who presented to our emergency department with persistent headache and ptosis over several weeks. Computed tomography angiography revealed ipsilateral carotid dissection and the patient was admitted for further management. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: The pathologies underlying Horner's syndrome are exceedingly diverse. Although classic teaching often focuses on neoplastic causes, and more specifically Pancoast tumors, neoplasms are discovered only in a small minority of Horner's syndrome cases. Other etiologies include trauma, cervical artery dissection, and infarction. With a better understanding of the pertinent anatomy and array of possible etiologies, emergency physicians may have more success in identifying and treating the causes of Horner's syndrome.

Síndrome de Horner contralateral asociado a bloqueo de ganglio estrellado: reporte de caso y revisión de la literatura / Contralateral Horner's syndrome associated with stellate ganglion block: case report and literature review

Se describe un caso de síndrome de Horner contralateral luego de bloqueo de ganglio estrellado. Se trata de un varón de 56 años con diagnóstico de síndrome doloroso regional complejo tipo II en miembro superior derecho quien posterior a la aplicación de anestésico local guiado por ecografía en proximidad al ganglio estrellado derecho presenta síndrome de Horner izquierdo. El síndrome de Horner contralateral a un bloqueo de ganglio estrellado es una entidad de ocurrencia supremamente rara, en nuestra práctica se presentó uno de los pocos casos reportados en la literatura, de interés para la comunidad científica (AU)

We describe a case of contralateral Horner’s syndrome following stellate ganglion block. A 56 years old man diagnosed with complex regional pain syndrome type II in right upper arm, who developed after the application of local anesthetic guided by ultrasound in proximity to the right stellate ganglion presented left Horner’s syndrome. The contralateral Horner’s syndrome following stellate ganglion block is a rare entity. In our practice occurred one of the few cases reported in the literature, which is of great interest for the medical community (AU)

The prognostic value of concurrent Horner syndrome in extended Erb obstetric brachial plexus palsy.

Horner syndrome may be seen in infants with extended Erb obstetric brachial plexus palsy. However, its prognostic value in these infants has not been previously investigated. A total of 220 infants with extended Erb palsy were included and divided into 2 groups: group I (n = 209) were infants with extended Erb palsy without Horner syndrome, and group II (n = 11) were infants with extended Erb palsy and concurrent Horner syndrome. The rate of good spontaneous recovery of elbow flexion was 59% in group I and 27% in group II, and the difference was significant (P = .038). The rate of good spontaneous recovery of wrist extension was 61% in group I and 0% in group II, and the difference as highly significant (P < .0001). Concurrent Horner syndrome in infants with extended Erb palsy may be considered as a poor prognostic sign for recovery of the sixth and seventh cervical roots.

Long lasting dysautonomia due to botulinum toxin B poisoning: clinical-laboratory follow up and difficulties in initial diagnosis.

BACKGROUND: Botulism is an acute form of poisoning caused by one of four types (A, B, E, F) toxins produced by Clostridium botulinum, ananaerobic, spore forming bacillus. Usually diagnosis of botulism is considered in patients with predominant motor symptoms: muscle weakness with intact sensation and preserved mental function. CASE PRESENTATION: We report a case of 56-year-old Caucasian female with a history of arterial hypertension, who presented with acute respiratory failure and bilateral ptosis misdiagnosed as brainstem ischemia. She had severe external and internal ophtalmoplegia, and autonomic dysfunction with neither motor nor sensory symptoms from upper and lower limbs. Diagnosis of botulinum toxin poisoning was made and confirmed by serum antibody testing in the mouse inoculation test. CONCLUSIONS: Ophtalmoplegia, autonomic dysfunction and respiratory failure can be caused by botulism. Early treatment and intensive care is essential for survival and recovery. The electrophysiological tests are crucial to correct and rapid diagnosis. Botulism (especially type B) should be considered in any case of acute or predominant isolated autonomic dysfunction.