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{{SK}} Wallenberg's syndrome; posterior inferior cerebellar artery syndrome
{{SK}} Wallenberg's syndrome; posterior inferior cerebellar artery syndrome (PICA)


==Overview==
==Overview==
Lateral medullary syndrome is a neurological condition caused by a stroke in the vertebral or posterior inferior [[cerebellar artery]] of the [[brain stem]].  
The [[lateral medullary syndrome]] is one of the most common clinical syndromes of [[brain stem]] caused by the decreased blood supply to the [[lateral medulla]]. It is also commonly known as [[Wallenberg's syndrome]] or [[posterior inferior cerebellar artery syndrome (PICA)]]. The most common cause is [[thromboembolic]] occlusion of [[vertebral arteries]]. It was described in 1895. The [[lateral medullary syndrome]] is basically a manifestation of the vaso-occlusive disease of [[intracranial vertebral arteries]] (ICVA) such as [[vertebral artery]] or [[posterior inferior cerebellar artery]]. The various pathophysiologic mechanisms involved can include; [[atherosclerosis]], athero-embolic phenomenon (heart, [[aorta]], or [[vertebral arteries]]), [[dissection]] and increased vascular tortuosity, vascular insufficiency, [[Virchow’s triad]] play an important role in understanding the pathogenesis of Wallenberg's syndrome.  


==Historical Perspective==
==Historical Perspective==
This syndrome was first described in 1808 by Gaspard Viesseux,<ref>{{WhoNamedIt|synd|1778}}</ref>. First descriptions by Adolf Wallenberg were in 1895 (clinical) and 1901 (autopsy findings).


==Pathophysiology==
* Gaspard Vieusseux, in 1808, was the first person to describe Wallenberg's syndrome.<ref name="pmid25817616">{{cite journal |vauthors=Ogawa K, Suzuki Y, Oishi M, Kamei S |title=Clinical study of 46 patients with lateral medullary infarction |journal=J Stroke Cerebrovasc Dis |volume=24 |issue=5 |pages=1065–74 |date=May 2015 |pmid=25817616 |doi=10.1016/j.jstrokecerebrovasdis.2015.01.006 |url=}}</ref>
The syndrome results from occlusion of the [[posterior inferior cerebellar artery]] ([[PICA]]) or one of its branches or of the [[vertebral artery]], in which the lateral part of the [[medulla oblongata]] infarcts.
*This syndrome was later on further elaborated by Adolf Wallenberg, in 1895.<ref name="pmid25817616">{{cite journal |vauthors=Ogawa K, Suzuki Y, Oishi M, Kamei S |title=Clinical study of 46 patients with lateral medullary infarction |journal=J Stroke Cerebrovasc Dis |volume=24 |issue=5 |pages=1065–74 |date=May 2015 |pmid=25817616 |doi=10.1016/j.jstrokecerebrovasdis.2015.01.006 |url=}}</ref>
*Thomas William was the first person to document extensive [[anatomy and physiology]] of [[brain stem]], the [[cerebellum]], and the [[ventricles]] in the 17th century. He performed [[necropsies]] and extensive dissections on his patient's brains.
* Joseph Jules Dejerine (1849–1917) and his wife  Dejerine-Klumpke demonstrated extensive visual illustrations of the various [[brain stem]] and cerebellar lesions.
* Charles Foix (1882–1927) was the first person to write an extensive case series on posterior cerebral arteries occlusion related syndromes and lateral medullary syndrome.
*Vertebral Basal Insufficiency (VBI) was first introduced by clinicians at the Mayo Clinic, Bob Siekert and Clark Millikan in 1970s.


==Natural History, Complications and Prognosis==
== Pathophysiology ==
The outlook for someone with lateral medullary syndrome depends upon the size and location of the area of the brain stem damaged by the stroke. Some individuals may see a decrease in their symptoms within weeks or months. Others may be left with significant neurological disabilities for years after the initial symptoms appeared.
The lateral medullary syndrome is basically a manifestation of the vaso-occlusive disease of [[Intracranial hemorrhage|intracranial]] [[vertebral arteries]] (ICVA) such as vertebral artery or posterior inferior cerebellar artery. The various pathophysiologic mechanisms involved can include;<ref name="pmid27960164">{{cite journal |vauthors=Kim JS, Caplan LR |title=Clinical Stroke Syndromes |journal=Front Neurol Neurosci |volume=40 |issue= |pages=72–92 |date=2016 |pmid=27960164 |doi=10.1159/000448303 |url=}}</ref><ref name="pmid25692102">{{cite journal |vauthors=Caplan LR |title=Lacunar infarction and small vessel disease: pathology and pathophysiology |journal=J Stroke |volume=17 |issue=1 |pages=2–6 |date=January 2015 |pmid=25692102 |pmc=4325635 |doi=10.5853/jos.2015.17.1.2 |url=}}</ref>
 
*[[Atherosclerosis]]
* Athero-embolic phenomenon (heart, aorta, or vertebral arteries)
*[[Dissection]] and increased vascular tortuosity
*Vascular insufficiency
*Virchow’s triad play an important role in understanding the pathogenesis of Wallenberg's syndrome
**An abnormality of the intima and vascular wall
**An abnormality of blood flow, and
**An abnormality of blood coagulability
 
Involvement of various structures in lateral medulla along with respective manifestation or clinical signs include;
 
* Nucleus ambiguous: [[dysphagia]], [[dysphonia]], and [[dysarthria]], [[laryngeal]], [[pharyngeal]] and palatal paralysis
* Trigeminal nucleus: ipsilateral facial and corneal anesthesia
*[[Spinothalamic tract]]: loss of pain and temperature sensation to the opposite side of the body
*[[Cerebellum]]: [[ataxia]]
*[[Hypothalamic]] fibers: [[sympathetic nervous system]] abnormal c/w [[Horner syndrome|Horners syndrome]]
* Deiters' nucleus and other [[vestibular nuclei]]: [[nystagmus]] and [[vertigo]]
* Central tegmental tract: palatal [[myoclonus]]
 
== Causes ==
 
*[[Atherosclerosis]] (VA>PICA>Medullary arteries)<ref name="pmid30459855">{{cite journal |vauthors=Inamasu J, Nakae S, Kato Y, Hirose Y |title=Clinical Characteristics of Cerebellar Infarction Due to Arterial Dissection |journal=Asian J Neurosurg |volume=13 |issue=4 |pages=995–1000 |date=2018 |pmid=30459855 |pmc=6208259 |doi=10.4103/ajns.AJNS_373_16 |url=}}</ref>
*[[Embolism]]
*[[Dissection]] (especially in younger patients)
*[[Dolichoectasias|Dolichoectasia]]
*[[Vasospasm]]
 
== Risk Factors ==
 
*Uncontrolled [[Hypertension, systemic|hypertension]]
*[[Smoking (patient information)|Smoking]]
*[[Diabetes mellitus|Diabetes]]
*Neck manipulation or injury
*[[Marfan syndrome]]
*[[Ehlers Danlos syndrome]]
*Fibromuscular dysplasia.
*
 
== Natural History, Complications and Prognosis ==
 
* The natural history, complications, and prognosis of Lateral medullary syndrome depends upon the size and location of the infarct/hemorrhagic area of the [[medulla]].
* Some people may experience a gradual improvement in their symptoms with complete resolution of the symptoms within the week to months while others may worsen or show no improvement despite the treatment.
*Overall, the prognosis is good and most of the patients are able to return back to a normal baseline. [[Ataxia]] is seen as the most common sequelae.
*The most common complications seen are;
**[[Aspiration pneumonia]]
**[[Deep vein thrombosis]]
**[[Pulmonary embolism]]
**[[Myocardial infarction]]


== Diagnosis ==
== Diagnosis ==
===Symptoms===
===History and Physical Examination===
Symptoms include
 
*[[Difficulties with swallowing]]
*[[Rostral]] lesions present as marked [[dysphagia]] and [[dysphonia]] (nucleus ambiguous)
*[[Hoarseness]]
*[[Caudally|Caudal]] lesion present as [[vertigo]], [[ataxia]], [[nausea]] and [[vomiting]], and [[Horner syndrome]]
 
==== Ipsilateral (same side of lesion): ====
 
*[[Ageusia]] or [[loss of taste]] on one side of the [[tongue]]
*[[Ataxia]] or [[incoordination]]<ref name="pmid2389292">{{cite journal |vauthors=Ferbert A, Brückmann H, Drummen R |title=Clinical features of proven basilar artery occlusion |journal=Stroke |volume=21 |issue=8 |pages=1135–42 |date=August 1990 |pmid=2389292 |doi=10.1161/01.str.21.8.1135 |url=}}</ref>
*[[Diplopia]] or [[double vision]]<ref name="pmid19269682">{{cite journal |vauthors=Kim YK, Schulman S |title=Cervical artery dissection: pathology, epidemiology and management |journal=Thromb. Res. |volume=123 |issue=6 |pages=810–21 |date=April 2009 |pmid=19269682 |doi=10.1016/j.thromres.2009.01.013 |url=}}</ref>
*[[Oscillopsia]]
*[[Dizziness]]
*[[Dizziness]]
*[[Dysphagia]] or [[difficulties with swallowing]]
*[[Dysphonia]] or [[hoarseness]]
*[[Dysarthria]] or [[slurred speech]]
*[[Ipsilateral]] sensory  deficits (pain and temperature sensation) affecting the face and [[cranial nerves]]
**absence of pain on the ipsilateral side of the face, as well as an absent [[corneal reflex]] (Damage to the spinal [[trigeminal nucleus]])
*[[Horner's syndrome]]
*Ipsilateral [[Vocal cord paralysis|vocal fold paralysis]]
*[[Palatal]] and [[pharyngeal]] [[paresis]]
*Palatal [[myoclonus]]
*[[Hiccups]]
*[[Hiccups]]
*[[Impaired gait]]
*[[Hoarseness]]
*[[Impaired coordination]]
*[[Nystagmus]]
*[[Lack of pain and temperature sensation on only one side of the face]] ([[Hypesthesia]])
*[[Vertigo]]
*[[Loss of taste]] on one side of the tongue
 
*[[Nystagmus]] ([[rapid involuntary movements of the eyes]])
====Contralateral (opposite side of lesion):====
*[[Nausea and vomiting]]
 
*Sense that the world is tilting
*[[Contralateral]] sensory deficits (pain and temperature sensation) affecting the trunk and extremities
*No or minimal [[hemiparesis]]
 
=== Evaluation: ===
 
==== Differential Diagnosis: ====
 
*[[Hemorrhagic stroke]]
*[[Multiple sclerosis]]
* Acute [[labyrinthitis]]<ref name="pmid28471903">{{cite journal |vauthors=Saber Tehrani AS, DeSanto JR, Kattah JC |title=Neuroimaging "HINTS" of the Lateral Medullary Syndrome |journal=J Neuroophthalmol |volume=37 |issue=4 |pages=403–404 |date=December 2017 |pmid=28471903 |doi=10.1097/WNO.0000000000000530 |url=}}</ref><ref name="pmid27619651">{{cite journal |vauthors=Chen K, Schneider AL, Llinas RH, Marsh EB |title=Keep it simple: vascular risk factors and focal exam findings correctly identify posterior circulation ischemia in "dizzy" patients |journal=BMC Emerg Med |volume=16 |issue=1 |pages=37 |date=September 2016 |pmid=27619651 |pmc=5020437 |doi=10.1186/s12873-016-0101-6 |url=}}</ref>
* Chronic pain syndrome
*[[Middle cerebral artery]] stroke
*[[Migraine]] headache
* Posterior reversible [[encephalopathy]] syndrome
*[[Subarachnoid hemorrhage]]
*[[Subdural hematoma]]
*[[Systemic lupus erythematosus]]
 
{| class="wikitable"
|+
!
! colspan="6" |History and Physical
!PMHx
!Diagnostic testing
|-
!
!Sensory deficits
!Motor deficits
!central vertigo
!peripheral vertigo
!Dizziness
!Ataxia
!
!
|-
|[[Hemorrhagic stroke]]
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| +/-
|<nowiki>-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|Hx of anticoagulant use
|CT w/o contrast
|-
|[[Multiple sclerosis]]
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|Younger female and known history of demyelinating disease
|MRI
|-
|Acute [[labyrinthitis]]
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
|Middle ear infection
|Positive Head thrust test
|-
|Chronic pain syndrome
|<nowiki>+/-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|Chronic back pain, arthropathy
|No specific diagnostic testing
|-
|[[Middle cerebral artery]] stroke
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|HTN, smokiong, DM, a fib
|CT w/o contrast
|-
|[[Migraine]] headache
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|hemicranial headaches
|clinical
|-
|[[Subarachnoid hemorrhage]]
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|HTN, ADPKD, CTD
|CT w/o contrast
|-
|[[Subdural hematoma]]
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|Hx of trauma
|CT w/o contrast
|-
|[[Systemic lupus erythematosus]]
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|PMHx of rash, arthropathy
|ANA, dsDNA
|}


===Physical Examination===
==== Diagnostic Tests: ====
====Neurologic====
*Sensory deficits affecting the trunk and extremities on the opposite side of the infarct
*Sensory and motor deficits affecting the face and cranial nerves on the same side with the infarct.
*[[Ataxia]]
*[[Nystagmus]],
*[[Horner's syndrome]]
*Damage to the spinal [[trigeminal nucleus]] causes absence of pain on the ipsilateral side of the face, as well as an absent [[corneal reflex]]


===MRI===
*[[MRI]] is the best diagnostic test to establish the diagnosis of Wallenberg's syndrome resulting from an infarct.<ref name="pmid28095387">{{cite journal |vauthors=De Cocker LJ, Lövblad KO, Hendrikse J |title=MRI of Cerebellar Infarction |journal=Eur. Neurol. |volume=77 |issue=3-4 |pages=137–146 |date=2017 |pmid=28095387 |doi=10.1159/000455229 |url=}}</ref>
[[Image:Wallenberganon_Image001.jpg|thumb|left|Clinical B1000 diffusion weighted MRI image showing an acute left sided dorsal lateral medullary infarct]]
*[[CT angiography|CTA]] and [[MRA]] can also be done to determine the vascular occlusion sites and to rule out dissection.<ref name="pmid26419965">{{cite journal |vauthors=Makin SD, Doubal FN, Dennis MS, Wardlaw JM |title=Clinically Confirmed Stroke With Negative Diffusion-Weighted Imaging Magnetic Resonance Imaging: Longitudinal Study of Clinical Outcomes, Stroke Recurrence, and Systematic Review |journal=Stroke |volume=46 |issue=11 |pages=3142–8 |date=November 2015 |pmid=26419965 |pmc=4617292 |doi=10.1161/STROKEAHA.115.010665 |url=}}</ref>
{{clr}}
* An [[EKG]] should be done to rule out any underlying thromboembolic phenomenon such as [[afib]].


===Localization of the Lesion===
=== Localization of the Lesion ===
{| class="wikitable"
{| class="wikitable"
| '''Dysfunction''' || '''Effects'''  
| '''Dysfunction''' || '''Effects'''  
Line 74: Line 259:
  | central tegmental tract || [[palatal myoclonus]]
  | central tegmental tract || [[palatal myoclonus]]
|}
|}
An affected person may present with [[ataxia]] on the side of lesion. [[Hiccups]] are another common sign.


==Treatment==
==Treatment==
Treatment for lateral medullary syndrome is symptomatic. A feeding tube may be necessary if swallowing is very difficult.  Speech/swallowing therapy  may be beneficial. In some cases, medication may be used to reduce or eliminate pain.  Some doctors report that the anti-epileptic drug gabapentin appears to be an effective medication for individuals with chronic pain.


==See Also==
* An interprofessional approach, aiming at a rapid response and coordinated team effort, involving neurologist, neurology specialty nurse, and the pharmacist has shown improved outcomes.<ref name="pmid29515427">{{cite journal |vauthors=Malik MT, Kenton Iii EJ, Vanino D, Dalal SS, Zand R |title=Lateral Medullary Ischemic Infarct Caused by Posterior Inferior Cerebellar Artery Aneurysm |journal=Case Rep Neurol |volume=9 |issue=3 |pages=316–319 |date=2017 |pmid=29515427 |pmc=5836213 |doi=10.1159/000485121 |url=}}</ref><ref name="pmid26732690">{{cite journal |vauthors=Nesbitt J, Moxham S, Ramadurai G, Williams L |title=Improving pain assessment and managment in stroke patients |journal=BMJ Qual Improv Rep |volume=4 |issue=1 |pages= |date=2015 |pmid=26732690 |pmc=4645684 |doi=10.1136/bmjquality.u203375.w3105 |url=}}</ref><ref name="pmid25355838">{{cite journal |vauthors=Meschia JF, Bushnell C, Boden-Albala B, Braun LT, Bravata DM, Chaturvedi S, Creager MA, Eckel RH, Elkind MS, Fornage M, Goldstein LB, Greenberg SM, Horvath SE, Iadecola C, Jauch EC, Moore WS, Wilson JA |title=Guidelines for the primary prevention of stroke: a statement for healthcare professionals from the American Heart Association/American Stroke Association |journal=Stroke |volume=45 |issue=12 |pages=3754–832 |date=December 2014 |pmid=25355838 |pmc=5020564 |doi=10.1161/STR.0000000000000046 |url=}}</ref>
[[Stroke_recovery#Lateral_Medullary_Syndrome|Stroke Recovery]]
*Treatment of Wallenberg's syndrome, like other stroke management, is aimed to achieve 3 goals
**Reducing the size of infarction
**Preventing any medical complication
**Improving patient outcome and prognosis
* Management includes:
** IV [[Thrombolytics]]<ref name="pmid28258876">{{cite journal |vauthors=Salerno A, Cotter BV, Winters ME |title=The Use of Tissue Plasminogen Activator in the Treatment of Wallenberg Syndrome Caused by Vertebral Artery Dissection |journal=J Emerg Med |volume=52 |issue=5 |pages=738–740 |date=May 2017 |pmid=28258876 |doi=10.1016/j.jemermed.2017.01.025 |url=}}</ref>
***[[Tissue plasminogen activator]] (TPA) within 3-4.5 hours
** Endovascular [[revascularization]]
*** For larger intracranial vessels
**[[Carotid endarterectomy]]
*** For larger extracranial vessels
** Antithrombotics has a controversial role in the setting of an acute stroke but have shown improved outcomes when combined with aspirin
*** Oral [[anticoagulants]] and [[antiplatelet agents]] should be considered upon discharge for secondary prevention of stroke
** High dose [[statins]]
** Close ICU monitoring for first 24 hrs after giving TPA
*** Blood pressure monitoring, allow permissive [[hypertension]] and lower the BP only if,
**** BP > 220/120 mmHg
**** Patient receives IV TPA
*** Normal saline is preferred for IV fluids and hypotonic fluids should be avoided to prevent [[cerebral edema]]
** Speech therapy to assess the risk of [[aspiration]]. A feeding tube or PEG tube may be considered for patients with severe [[dysphagia]].
** Low dose heparin or low molecular weight heparin (LWMH) for [[DVT prophylaxis]]
** Physical therapy and Occupational therapy <br />


==References==
==References==
<references/>
<references />


==External links==
==External links==
Line 90: Line 293:


{{Diseases of the nervous system}}
{{Diseases of the nervous system}}
{{Lesions of spinal cord and brainstem}}
{{Lesions of the spinal cord and brainstem}}


[[Category:Neurology]]
[[Category:Neurology]]
[[Category:Disease]]


[[de:Wallenberg-Syndrom]]
[[de:Wallenberg-Syndrom]]

Latest revision as of 04:55, 10 August 2020

Lateral medullary syndrome
The three major arteries of the cerebellum: the SCA, AICA, and PICA. (Posterior inferior cerebellar artery is PICA.)
ICD-10 G46.3
DiseasesDB 10449
MeSH D014854

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sabeeh Islam, MBBS[2]

Synonyms and keywords: Wallenberg's syndrome; posterior inferior cerebellar artery syndrome (PICA)

Overview

The lateral medullary syndrome is one of the most common clinical syndromes of brain stem caused by the decreased blood supply to the lateral medulla. It is also commonly known as Wallenberg's syndrome or posterior inferior cerebellar artery syndrome (PICA). The most common cause is thromboembolic occlusion of vertebral arteries. It was described in 1895. The lateral medullary syndrome is basically a manifestation of the vaso-occlusive disease of intracranial vertebral arteries (ICVA) such as vertebral artery or posterior inferior cerebellar artery. The various pathophysiologic mechanisms involved can include; atherosclerosis, athero-embolic phenomenon (heart, aorta, or vertebral arteries), dissection and increased vascular tortuosity, vascular insufficiency, Virchow’s triad play an important role in understanding the pathogenesis of Wallenberg's syndrome.

Historical Perspective

  • Gaspard Vieusseux, in 1808, was the first person to describe Wallenberg's syndrome.[1]
  • This syndrome was later on further elaborated by Adolf Wallenberg, in 1895.[1]
  • Thomas William was the first person to document extensive anatomy and physiology of brain stem, the cerebellum, and the ventricles in the 17th century. He performed necropsies and extensive dissections on his patient's brains.
  • Joseph Jules Dejerine (1849–1917) and his wife Dejerine-Klumpke demonstrated extensive visual illustrations of the various brain stem and cerebellar lesions.
  • Charles Foix (1882–1927) was the first person to write an extensive case series on posterior cerebral arteries occlusion related syndromes and lateral medullary syndrome.
  • Vertebral Basal Insufficiency (VBI) was first introduced by clinicians at the Mayo Clinic, Bob Siekert and Clark Millikan in 1970s.

Pathophysiology

The lateral medullary syndrome is basically a manifestation of the vaso-occlusive disease of intracranial vertebral arteries (ICVA) such as vertebral artery or posterior inferior cerebellar artery. The various pathophysiologic mechanisms involved can include;[2][3]

  • Atherosclerosis
  • Athero-embolic phenomenon (heart, aorta, or vertebral arteries)
  • Dissection and increased vascular tortuosity
  • Vascular insufficiency
  • Virchow’s triad play an important role in understanding the pathogenesis of Wallenberg's syndrome
    • An abnormality of the intima and vascular wall
    • An abnormality of blood flow, and
    • An abnormality of blood coagulability

Involvement of various structures in lateral medulla along with respective manifestation or clinical signs include;

Causes

Risk Factors

Natural History, Complications and Prognosis

  • The natural history, complications, and prognosis of Lateral medullary syndrome depends upon the size and location of the infarct/hemorrhagic area of the medulla.
  • Some people may experience a gradual improvement in their symptoms with complete resolution of the symptoms within the week to months while others may worsen or show no improvement despite the treatment.
  • Overall, the prognosis is good and most of the patients are able to return back to a normal baseline. Ataxia is seen as the most common sequelae.
  • The most common complications seen are;

Diagnosis

History and Physical Examination

Ipsilateral (same side of lesion):

Contralateral (opposite side of lesion):

  • Contralateral sensory deficits (pain and temperature sensation) affecting the trunk and extremities
  • No or minimal hemiparesis

Evaluation:

Differential Diagnosis:

History and Physical PMHx Diagnostic testing
Sensory deficits Motor deficits central vertigo peripheral vertigo Dizziness Ataxia
Hemorrhagic stroke + + +/- - +/- +/- Hx of anticoagulant use CT w/o contrast
Multiple sclerosis + + +/- - - - Younger female and known history of demyelinating disease MRI
Acute labyrinthitis + - - + + +/- Middle ear infection Positive Head thrust test
Chronic pain syndrome +/- - - - - - Chronic back pain, arthropathy No specific diagnostic testing
Middle cerebral artery stroke + + - - - - HTN, smokiong, DM, a fib CT w/o contrast
Migraine headache + + - - - - hemicranial headaches clinical
Subarachnoid hemorrhage - - - - + - HTN, ADPKD, CTD CT w/o contrast
Subdural hematoma + + - - + - Hx of trauma CT w/o contrast
Systemic lupus erythematosus +/- +/- - - - - PMHx of rash, arthropathy ANA, dsDNA

Diagnostic Tests:

  • MRI is the best diagnostic test to establish the diagnosis of Wallenberg's syndrome resulting from an infarct.[9]
  • CTA and MRA can also be done to determine the vascular occlusion sites and to rule out dissection.[10]
  • An EKG should be done to rule out any underlying thromboembolic phenomenon such as afib.

Localization of the Lesion

Dysfunction Effects
lateral spinothalamic tract contralateral deficits in pain and temperature sensation from body
spinal trigeminal nucleus ipsilateral loss of pain and temperature sensation from face
nucleus ambiguus (which affects vagus X and glossopharyngeal nerves IX) dysphagia, hoarseness, diminished gag reflex
vestibular system vertigo, diplopia, nystagmus, vomiting
descending sympathetic fibers ipsilateral Horner's syndrome
central tegmental tract palatal myoclonus

Treatment

  • An interprofessional approach, aiming at a rapid response and coordinated team effort, involving neurologist, neurology specialty nurse, and the pharmacist has shown improved outcomes.[11][12][13]
  • Treatment of Wallenberg's syndrome, like other stroke management, is aimed to achieve 3 goals
    • Reducing the size of infarction
    • Preventing any medical complication
    • Improving patient outcome and prognosis
  • Management includes:
    • IV Thrombolytics[14]
    • Endovascular revascularization
      • For larger intracranial vessels
    • Carotid endarterectomy
      • For larger extracranial vessels
    • Antithrombotics has a controversial role in the setting of an acute stroke but have shown improved outcomes when combined with aspirin
    • High dose statins
    • Close ICU monitoring for first 24 hrs after giving TPA
      • Blood pressure monitoring, allow permissive hypertension and lower the BP only if,
        • BP > 220/120 mmHg
        • Patient receives IV TPA
      • Normal saline is preferred for IV fluids and hypotonic fluids should be avoided to prevent cerebral edema
    • Speech therapy to assess the risk of aspiration. A feeding tube or PEG tube may be considered for patients with severe dysphagia.
    • Low dose heparin or low molecular weight heparin (LWMH) for DVT prophylaxis
    • Physical therapy and Occupational therapy

References

  1. 1.0 1.1 Ogawa K, Suzuki Y, Oishi M, Kamei S (May 2015). "Clinical study of 46 patients with lateral medullary infarction". J Stroke Cerebrovasc Dis. 24 (5): 1065–74. doi:10.1016/j.jstrokecerebrovasdis.2015.01.006. PMID 25817616.
  2. Kim JS, Caplan LR (2016). "Clinical Stroke Syndromes". Front Neurol Neurosci. 40: 72–92. doi:10.1159/000448303. PMID 27960164.
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External links

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