Loop Of Posterior Inferior Cerebellar Artery Research Articles

Outcome of Endoscope-Assisted Microvascular Decompression in Patients With Hemifacial Spasm Caused by Severe Indentation of the Brain Stem at the Pontomedullary Sulcus by the Posterior Inferior Cerebellar Artery.

Microvascular decompression (MVD) is the most effective treatment option for hemifacial spasm (HFS). However, deeply located forms of compression would require proper identification to allow for adequate decompression. To describe the usefulness of endoscopic visualization in one of the most challenging compression patterns in HFS, where the posterior inferior cerebellar artery (PICA) loop is severely indenting the brain stem at the proximal root exit zone of facial nerve along the pontomedullary sulcus. Radiological and operative data were checked for all patients in whom severe indentation of the brainstem by PICA at pontomedullary sulcus was recorded and endoscope-assisted MVD was performed. Clinical correlation and outcome were analyzed. A total of 58 patients with HFS were identified with radiological and surgical evidence proving brainstem indentation at the VII transitional zone. In 31 patients, PICA was the offending vessel to the facial nerve. In 3 patients, the PICA loop was mobilized under visualization of a 45° endoscope. A total of 31 patients had a mean follow-up duration of 52.1 mo. The mean duration between start of complaints and surgery was 7.2 yr. In the last follow-up, all patients had remarkable spasm improvement. A total of 5 patients had more than 90% disappearance of spasms and 26 patients experienced spasm-free outcome. Although severe indentation of brain stem implies morphological damage, outcome after MVD is excellent. A 45° endoscope is extremely helpful to identify compression down at the pontomedullary sulcus. Deeply located compression site can easily be missed with microscopic inspection alone.

THE CAUSE OF SELDOM INCIDENCE OF GLOSSOPHARINGEAL NERVE NEURALGIA

Trigeminal neuralgia (TN) and glossopharyngeal neuralgia (GN) are caused by compression of the roots of these nerves by adjacent vessels – neurovascular conflict. The purpose of the research was to study the topographic and anatomical relationship of the trigeminal nerve root (TNR) with the superior cerebellar artery and the glossopharyngeal nerve root (GNR) with the posterior inferior cerebellar artery, and to assess the impact of anatomical pattern on frequency of glossopharyngeal and trigeminal neuralgia occurring. Topographic and anatomical relationship of glossopharyngeal and trigeminal nerves with adjacent arteries was studied in 50 anatomic specimens (in sito) of persons who did not suffer from trigeminal or glossopharyngeal neuralgia. The specifics of neurovascular conflict in 4 patients with glossopharyngeal neuralgia were also analyzed during microvascular decompression surgery. The superior cerebellar artery loop crossed the surface of the trigeminal nerve root in 44 % of anatomical specimens of subjects without neuralgia during life-time. In a case of age vessel dolichoectasia the peak of the arterial loop would be located below the upper edge of the trigeminal nerve root resulting in the neurovascular conflict. In most anatomical specimens the posterior inferior cerebral artery loop was located collateral to the glossopharyngeal nerve root, preventing development of neurovascular conflict. Only in one of the 50 specimens the artery loop was placed at an angle with the glossopharyngeal nerve. In patients with glossopharyngeal neuralgia microvascular decompression surgery revealed that the distal arm of the posterior inferior cerebellar artery loop was located at an angle with the glossopharyngeal nerve root. Thus, the special topographic and anatomical relationship between the glossopharyngeal nerve and the posterior cerebellar artery cause much rarer occurrence of the glossopharyngeal neuralgia in comparison with the trigeminal neuralgia.

A Painful Pause

An 83-year-old man had lancinating throat pain, triggered by swallowing, coughing, and even speaking. He would pass out with excruciating pain. Magnetic resonance imaging showed an abnormal posterior inferior cerebellar artery loop (PICA) (left, arrow) exiting the brainstem (left, arrowhead), near the left glossopharyngeal and vagus nerves. Arterial compression from the posterior inferior cerebellar artery on the cranial nerves could produce demyelination, resulting in abnormal cross-conduction. Pain and syncope disappeared with carbamazepine treatment. Severe pain can cause vasovagal syncope,1 but direct vagal stimulation was responsible for asystole in our patient (right). A pacemaker will not prevent syncope if pain is associated with a vasovagal response.2

Vascular Compression as a Potential Cause of Occipital Neuralgia: A Case Report

Vascular compression is a well-established cause of cranial nerve neuralgic syndromes. A unique case is presented that demonstrates that vascular compression may be a possible cause of occipital neuralgia. A 48-year-old woman with refractory left occipital neuralgia revealed on magnetic resonance imaging and computed tomographic imaging of the upper cervical spine an atypically low loop of the left posterior inferior cerebellar artery (PICA), clearly indenting the dorsal upper cervical roots. During surgery, the PICA loop was interdigitated with the C1 and C2 dorsal roots. Microvascular decompression alone has never been described for occipital neuralgia, despite the strong clinical correlation in this case. Therefore, both sectioning the dorsal roots of C2 and microvascular decompression of the PICA loop were performed. Postoperatively, the patient experienced complete cure of her neuralgia. Vascular compression as a cause of refractory occipital neuralgia should be considered when assessing surgical options.

Microvascular decompression for hyperactive cranial nerve rhizopathies

Hyperactive dysfunction syndromes including trigeminal neuralgia, hemifacial spasm and glossopharyngeal neuralgia, may result from vascular loops distorting the intracranial portion of the affected nerves. Microvascular decompression has been recommended as treatment for these conditions. Posterior fossa exploration in 16 patients who presented with hyperactive cranial rhizopathies revealed vascular distortion of the relevant cranial nerve in 14 patients. Amongst patients with trigeminal neuralgia and superior cerebellar artery (SCA) was responsible in 4 cases, the anterior inferior cerebellar artery (AICA) in 2, an ectatic basilar artery in 2 and a vein was the cause in one patient with atypical facial pain. In two patients with combined trigeminal and glossopharyngeal neuralgia the posterior inferior cerebellar artery (PICA) was responsible for the glossopharyngeal pain and the SCA for the trigeminal neuralgia. One patient with classical glossopharyngeal neuralgia had a loop of PICA distorting the nerve. The facial nerve was indented by a loop of AICA in two patients with hemifacial spasm. Insertion of a muscle graft between the appropriate nerve and vessel gave relief in 14 patients which has been maintained at follow-up (l-20 months; mean 10 months). In patients experiencing glossopharyngeal neuralgia and glossopharyngeal nerve and upper two vagal nerve filaments were divided in addition to mobilising the loop of PICA. One patient suffered a myocardial infarction and died later. Post operative complications included severe headache (4 patients), confusion (2) and a superficial wound infection (1). Two patients required re-exploration for cerebrospinal fluid fistulae. Two patients complained of transient hyperaesthesiae related to the incision scar. One patient suffered sensorineural deafness which had only slightly improved at review. Trigeminal pain returned in two patients who had no evidence of neuro-vascular compression but re-exploration revealed an arterial loop (of AICA) which had been missed previously; mobilisation of this relieved the pain.