 Good morning everybody. My name is Dr. Muhammad Saleh. I am a third year PG resident in Department of Radiodiagnosis at GNMC Eleven. I will be presenting a case on neuro fibromatosis 2, which presented as a vocal cord palsy in a young child. So NF2 is a rare auto-dominant neuro-cutaneous disorder manifesting as a development of multiple CNS tumors. Patients with this disease have intra-cranial schwannomas, which are mostly vestibular intra-cranial and spinal meninjomas and intramedulary epindiomomas. The clinical presentation was a 15-year-old male presented with complaint of hoarseness of voice for past three months in pain in cervical neck region for past one month, which was radiating to right ocular and associated with numbness. No other comorbidities were present. One examination is vitals were stibular, pyridontal, rossoft and non-tender. His laryngoscopic evaluation showed light peritone and right vocal cord palsy. His imaging findings on MRI were there were bilateral cerebellum-contine angle solid mass region with intracranialic oral extension. Few intradural extramedulary mass regions were noted at cervical dorsal level and multiple small extramedulary nodular legions were noted at the lower thoracic and lumbar vertebral levons, which were likely schwannomas. There was a well-defined solid mass region in right carotid space, which was causing major displacement of the carotid vessels and spleen of the internal carotid artery and the internal jupylogin, which was such a strip of v-carotid schwannomas. These are the sagittic parts of the patient, in which we can see there are two well-defined even hyperintense T2-ISO2 hyperintense legions in the extramedulary region of the cervical spinal cord, which are causing significant mass break over the spinal cord. In the third image, we can see that there are multiple small well-defined nodular T2 hyperintense legions in the lower thoracic and lumbar vertebral levons. In this image, we can see that on the axial T1 post-contrast image, there is significant post-contrast enhancement of the legion, which is causing significant mass effect over the cervical spinal cord. The same winding can also be confirmed on the star core image. We can also see that there is a well-defined, enhancing solid mass legion noted in the region of the right carotid space, which is causing spleen of the internal jupylogin and the internal carotid artery. On the axial T2-IT images, we can see that there are bilateral CP angle solid mass legions with intra-canalic extensions. An axial T1 post-contrast image taken at a lower level shows the solid mass legion in the right carotid space region, which is causing spleen of the ICA and the IJV. So NF2 disease is rare with an estimated prevalence of 1 in 50,000. They usually present in young adults in the age group of 18 to 24 years. Of patients with NF2, 50% have an affected period, that is, they are autosomal dominant enteritis, and 50% have a denomination. NF2 is located on the long arm of those amounts 22 and encodes the merlin protein, plays a role in chronic inhibition of growth and has tumors of pressure function, at least in part according to this model. Although variably expressed throughout the body during human development, merlin is highly expressed in adrenal neuronal cells, shorn cells, and meningeal cells. So a mutation in NF2 causes the loss of protein function, resulting in predisposition to tumor formation throughout the nervous system. Although meningeomas are often isolated finding in adults, their presence in a child should raise the suspicion of NF2. The presence of multiple and different types of spinal tumors should also raise a high suspicion of NF2. The diagnostic criteria for NF2 has been established by a consensus of experts. A person is thought to have NF2 if they have vestibular shornomas in both years, that is, in bilateral CP angle shornomas, or if they have a vestibular shornoma on one side, and one or several cross-degree relatives with NF2. This is a table which shows the frequency of the lesions, which are commonly associated with NF2, and we can see that in the neurological lesions, bilateral vestibular shornomas and other cranial shornomas are common. Apart from this, spinal tumors, mostly extramedulary, are the common lesions. In ophthalmological lesions, cataracts are found in roughly 60-80% of these patients, and in the cutaneous lesions, approximately half of these patients will have some sort of skin tumor or skin blood present. This is the menstrual criteria for the diagnosis of NF2 and NF2, and it shows that if the patient has bilateral vestibular shornomas, no additional binding is needed. If there is a family history of NF2, then a unilateral vestibular shornomas or two NF2-associated lesions, which include meningioma, lioma, neurofibromas, shornomas or cataracts, are sufficient for the diagnosis. In unilateral vestibular shornomas, two NF2-associated lesions, such as meningiomas, gliomas, are sufficient, and if the patient has multiple meningiomas, then either a unilateral vestibular shornoma or two other NF2-associated lesions are needed for the diagnosis of NF2. Coming to vocal cord palsy, this is actually common in patients with NF2, but it is usually found in adults with rates comparable to those of other penile neuropathies. Previous two researches, which showed a cohort of 31 NF2 patients, which was done by best et al, found that 71% had evidence of unilateral or bilateral vocal fold motion impairment. Non-femetal found an 86% rate of vocal fold motion impairment in a group of 22 NF2 patients. Now this typically results from compression of the vagus nerve by neural tumors or surgical injury to the nerve during tumor resection and there are currently no reports of idiopathic vocal fold palsy in patients with NF2. Our patient developed vocal fold palsy due to vagal noshornoma. Another possibility is that the mobility impairment may have resulted from a subclinical peripheral neuropathy as these have been characterized in patients with NF2. Electrovisological evidence of peripheral neuropathy in the absence of tumor masses in NF2 patients has been demonstrated. Our patient's young age at presentation is unusual as the two previous studies of NF2 patients with vocal fold palsy included only adults. Perhaps the early onset of this possible peripheral neuropathy potentials are more aggressive disease schools in these patients given their young age and potential for disease progression. Patients have been managed with closed monitoring and conservative treatments. These were the references that were used in this reactase presentation of a young male presenting with vocal fold palsy, which came out to be a case of neurofagromatosis.