Monday, July 20, 2015

BRAINSTEM Stroke Syndromes


BRAINSTEM Stroke Syndromes

Brainstem stroke syndromes refer to a group of syndromes that occur secondary to occlusion of small perforating arteries of the posterior circulation. The resulted infarction has characteristic clinical picture according to the involved area however, generally there is ipsilateral cranial nerve palsy and contralateral hemiplegia/hemiparesis and sensory loss.


Medulla Oblongata


Lateral medullary syndrome, (or Wallenberg syndrome) is characterised by: 

  • ipsilateral deficits in pain and temperature over face (spinal trigeminal nucleus involvement) 
  • ataxia and in-coordination (inferior cerebellar peduncle) 
  • dysarthria/dysphagia/decreased gag (nucleus ambiguus) 
  • contralateral deficits in pain and temperature over trunks and limbs 
  • vertigo (vestibular nucleus)

Medial medullary syndrome, also known as Dejerine syndrome, represents less than 1% of brainstem stroke syndromes. Thrombotic or embolic occlusion of small perforating branches from vertebral or proximal basilar artery supplying the medial aspect of medulla oblongata cause this rare syndrome. It is characterized by contralateral hemiplegia/hemiparesis as well as hemisensory loss with ipsilateral hypoglossal palsy (ipsilateral tongue weakness and atrophy) from involvement of CN XII nucleus. Other manifestations e.g. vertigo, nausea, ipsilateral limb ataxia are also reported.

Hemimedullary syndrome, also known as Babinski-Nageotte syndrome, occurs as a result of the occlusion of the ipsilateral vertebral artery proximal to the posterior inferior cerebellar artery and its anterior spinal artery branches. This situation causes lateral medullary infarct and medial medullary infarct simultaneously.

Pons


Lateral pontine syndrome, also known as Marie-Foix syndrome, refers to one of the brainstem stroke syndromes which occurs due to occlusion of perforating branches of the basilar and anterior inferior cerebellar (AICA) arteries. This results in infarction of the lateral aspect of the pons which produces characteristic clinical picture from involvement of the following pontine structures: 
  • corticospinal tract leads to contralateral hemiplegia/hemiparesis. 
  • spinothalamic tract causes contralateral loss of pain and temperature sensation. 
  • cerebellar tracts causes ipsilteral limb ataxia. 
  • CN VII nucleus leads to ipsilateral facial paralysis. 
  • CN VIII vestibular and cochlear nuclei leads to ipsilateral hearing loss, vertigo and nystagmus. 

Inferior medial pontine syndrome (or Foville syndrome) is one of the brainstem stroke syndromes occurred when there is infarction of the medial inferior aspect of the pons due to occlusion of the paramedian branches of the basilar artery. This infarction involves the following: 
  • corticospinal tract leads to contralateral hemiplegia/hemiparesis. 
  • corticobulbar tract leads to contralateral weakness of the lower half of the face. 
  • medial leminiscus leads to contralateral loss of proprioception and vibration. 
  • middle cerebellar peduncle leads to ipsilateral ataxia. 
  • abducent nerve roots leads to lateral gaze paralysis and diplopia. 

Locked in syndrome (LIS) is a condition that can occur as a result of a stroke involving the brainstem; the stroke damages the ventral brainstem, corresponding to the pyramidal bundles. The infarct is pontine; the midbrain is preserved. The oculomotor nerve III is intact so the patient can open his/her eyes and vertical eye movements are preserved. The patient is conscious with preserved cognitive function but can not move or communicate to the complete paralysis of all voluntary muscles of the body. The patient is a high quadriplegic, impairment of corticobulbar tracts leads to paralysis of VII and VI. There is usually preservation of eyelid elevation and upward gaze. Respiratory insufficiency requires the use of mechanical ventilation.The most common cause of brainstem stroke is a thrombosis of the basilar artery. Other causes include but trauma or cardiocircolatory failure. 
  • ventral pontine syndromes 
  • ventral pontine syndrome (Raymond syndrome) 
  • ventral pontine syndrome (Millard-Gubler syndrome) 

Facial colliculus syndrome refers to a constellation of neurological signs due to a lesion at the facial colliculus, involving: 
  • abducens nerve (CN VI) nucleus 
  • facial nerve (CN VII) fibres at the genu 
  • medial longitudinal fasciculus 
and resulting in peripheral facial palsy and conjugate gaze palsy. 

The facial palsy is due to interruption of the ipsilateral facial nerve fibres at the genu as they arch behind the abducens nerve (CN VI) nucleus (thus forming the colliculus). 

The conjugate gaze palsy is due to involvement of innervation not only to the ipsilateral abducens nerve to lateral rectus, but also to the interneurons projecting into the medial longitudinal fasciculus which contribute to innervation of the contralateral medial rectus (thus coordinating conjugate gaze).

Midbrain


Weber syndrome is a midbrain stroke syndrome that involves the fascicles of the oculomotor nerve resulting in an ipsilateral CN III palsy and contralateral hemiplegia or hemiparesis. 

Benedikt syndrome, or paramedian midbrain syndrome, is a midbrain stroke syndrome that involves the fascicles of the oculomotor nerve and the red nucleus resulting in an ipsilateral CN III palsy and crossed hemiataxia and chorea. 

Using imaging alone, it is difficult to distinguish Benedikt from Weber syndrome, unless clear involvement of the red nucleus can be identified, which is seen in the former.

Claude syndrome is one of the brainstem stroke syndromes in which there is infarction of the dorsomedial aspect of the midbrain secondary to occlusion of the small perforating branches of the posterior cerebral artery supplying this area. The infarction involves the medial aspect of red nucleus with the rubrodentate fibers, CN III nucleus and superior cerebellar peduncle. Clinical picture is characteristic and includes ipsilateral oculomotor nerve palsy and contralateral upper and lower limb ataxia. 


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