The differential diagnosis for mass lesions causing neural foraminal widening and nerve root symptoms is wide

and includes both benign and malignant conditions (see Table 1). Table 1 Benign and malignant conditions causing spinal foraminal widening Benign conditions Benign peripheral nerve sheath tumour Tarlov cyst Spinal hydatid disease Tuberculous or pyogenic spondylitis Malignant conditions Malignant peripheral nerve sheath tumour Metastases/lymphoma Chordoma Solitary plasmacytoma

The commonest differential diagnosis is a peripheral nerve sheath tumour (PNST), which can be divided into benign (neurofibroma or schwannoma) and malignant categories. They are soft tissue tumours arising from the spinal nerve root and may have a dumbbell shape on MR imaging. They are slow-growing and plexiform neurofibromas can involve a long segment of nerve. They are usually of low signal intensity on T1- and of high signal intensity on T2weighted sequences [7]. The signal characteristics may be difficult to distinguish from endometriosis as lesions can appear heterogeneous if internal degeneration or necrosis is present, as is commonly identified in schwannomas. Malignant PNSTs grow more rapidly, show central necrosis

and have an ill-defined border [7]. Other benign differentials to be considered are tuberculosis, more commonly occurring in the cervical or thoracic spine. Uncommonly, hydatid cysts present with a lesion affecting a vertebral body as a result of a portovertebral shunt. They tend to be multicystic, cause bone destruction, but typically preserve the disc space and do not involve the spinal cord [8]. Chordomas are rare, aggressive malignant tumours arising from ectopic notochord remnants, especially in the sacro-coccygeal or spheno-occipital-clival regions. On MR imaging, they display low to intermediate signal intensity on T1- and very high signal intensity on T2-weighted sequences. Chordomas enhance heterogeneously and cause local bony destruction. Haemorrhagic necrosis can also occur within the tumour leading to areas of high signal on T1 [9].

Computed tomography (CT) and magnetic resonance imaging (MRI) reliably demonstrate typical features of schwannomas or neurofibromas in the vast majority of dumbbell lesions responsible for neural foraminal widening. However, a large variety of unusual lesions which are causes of neural foraminal widening can also be encountered in the spinal neural foramen. Radiologic findings can be helpful in differential diagnosis of lesions of spinal neural foramen including neoplastic lesions such as benign/malign peripheral nerve sheath tumors (PNSTs), solitary bone plasmacytoma (SBP), chondroid chordoma, superior sulcus tumor, metastasis and non-neoplastic lesions such as infectious process (tuberculosis, hydatid cyst), aneurysmal bone cyst (ABC), synovial cyst, traumatic pseudomeningocele, arachnoid cyst, vertebral artery tortuosity. In this article, we discuss CT and MRI findings of dumbbell lesions which are causes of neural foraminal widening.

A meningioma with intradural and extradural components occasionally mimic a nerve sheath tumor, or a nerve sheath tumor with a predominant intradural component may mimic a meningioma. However, nerve sheath tumors usually have hyperintensity on T2-weighted images, whereas meningiomas usually are isointense to the spinal cord on T2-weighted images. Most meningiomas are lateral or dorsal, whereas most nerve sheath tumors are ventral. Furthermore, a mass lesion with both intradural and extradural components is most likely to be a nerve sheath tumor.

Choroid plexus tumours

Choroid plexus tumours can be classified as primary or secondary neoplsms of the choroid plexus :

primary choroid plexus carcinoma (CPC) : 20% WHO Grade III choroid plexus papilloma (CPP) : 80% WHO Grade I intraventricular meningioma secondary o choroid plexus metastases
o o o

The distribution of tumours matches the distribution of choroid

y y y y

lateral ventricle : 50% fourth ventricle : 40% third ventricle : 5% multicentric : 5%

Differential diagnosis
The differential is essentially that of choroid plexus tumours.

choroid plexus carcinoma (CPC) : can be very difficult on imaging alone o heterogeneous contrast enhancement o may show parenchymal invasion o if parenchymal invasion is absent, then they are almost impossible to distinguish from CPP choroid plexus metastases

When located in the posterior fossa in children (less common) other tumours to be considered include :

y y y

medulloblastoma atypical teratoid / rhabdoid tumour (AT/RT) papillary anaplastic ependymoma

In adults consider :

y y y

intraventricular meningioma subependymoma / central neurocytoma exophytic glioma

Choroid plexus papilloma

A choroid plexus papilloma (CPP) is an uncommon, benign (WHO grade I for typical and WHO grade II for atypical) neuroepithelial intraventricular tumour which can occur in both the paediatric (commoner) and adult population.

Epidemiology
The tumours account for approximately 1% of all brain tumours, 2 - 6% of all paediatric brain tumours and 0.5% of the adult brain tumours. Approximately 85% of all choroid plexus papillomas occur in children under the age of 5 years 4 .

Clinical presentation
Significant hydrocephalus is very common - it is seen in over 80% of cases 4 . Although the exact mechanism remains uncertain, it is believed to be due to a combination of CSF over production and decreased arachnoid granulation resorption.

An association with von Hippel Lindau disease is recognised (rather than the more frequently associated haemangioblastoma).

Pathology
Choroid plexus papillomas typically appear as cauliflower like masses 4. Microscopically they demonstrate papillary structures with a delicate fibrovascular core lined by columnar or cuboidal epithelial cells with vesicular nuclei. Their appearance is very similar to normal choroid plexus.

Location
Unlike most other brain tumours, which are more common in the posterior fossa in children and supratentorial compartment in adults, the relationship is reversed for choroid plexus papillomas. In adults these tumours most often (70%) occur in the fourth ventricle. In the paediatric age group the lateral ventricles are the commonest location, with a predilection for the trigone. Third ventricular, cerebellopontine angle, parenchymal and even pineal region tumours have also been described.

Markers
y

cytokeratin : may help distinguish from an ependymoma

Radiographic features CT
The tumours are usually well-defined lobulated masses, either iso- or somewhat hyperdense compared to the adjacent brain. There is associated hydrocephalus. They usually homogeneously enhance, demonstrating with an irregular frond-like pattern, resulting in a cauliflower-like appearance. If there is markedly heteregeneous contrast enhancement, a choroid plexus carcinoma should be suspected 4.

Fine, speckled calcification is seen within the tumour in approximately 25% of cases 4 .

MRI
The frond-like morphology of the tumour can usually be seen, especially following contrast administration. Varying degrees of associated hydrocephalus are also present in almost all cases.

y y

y y

T1 : typically isointense c.f. to adjacent brain. May be somewhat hypointense T2 o iso to hyperintense o small flow-voids may be seen within the tumour T1 C+ (Gd) : marked enhancement, tends to be homogenous MR spectroscopy o decreased NAA o increased Cho

Angiography
Being very vascular tumours, these masses demonstrate intense vascular blush on angiography. Enlarged choroidal arteries may be seen feeding the tumour, with shunting 4 .

Treatment and prognosis

Total excision should be the aim of therapy and is curative in a vast majority of cases. CSF seeding / spread is uncommon.

WHO Grade 2 Cell of Origin: Neurons Common Locations: Intraventricular (Lat >> 3rd) (often attached to septum pellucidum) Demographics: Young adults (mean age: 25-30) Clinical Presentation: Nausea, vomiting, headache due to obstructive hydrocephalus. Histology: Uniform appearance of small, round cells mimics oligodendroglioma. Electron microscopy may demonstrate neuronal features. Special Stains: Purely neuronal origin demonstrated by neuronal markers (synaptophysin, neuronal specific enolase) and negativity to glial markers. Progression: Slow-growing, benign tumor; no extraventricular extension. Resection usually curative. Radiology: Well-circumscribed, lobulated intraventricular mass. Often (50%) with bulky calcifications, best demonstrated on CT. Isodense/slightly hyderdense on CT. May be isointense to gray matter on both T1 and T2-weighted MR images. MR often demonstrates small "cysts". Comments: Previously misdiagnosed as intraventricular oligodendroglioma. Rare reports of extraventricular (parenchymal) location. Rarely, spontaneous intraventricular hemorrhage.

Soft tissue lesions Signal Intensities on T1- and T2-weighted Images

High signal intensity on T1-weighted images plus intermediate signal intensity on T2-weighted images

Lipoma Liposarcoma

Lipoblastoma Hibernoma Elastofibroma Fibrolipohamartoma Metastasis of melanoma (melanin) Clear cell sarcoma (melanin) High signal intensity on T1-weighted images plus high signal intensity on T2-weighted images Hemangioma Lymphangioma Subacute hemangioma Small arteriovenous malformation

Low signal intensity on T1-weighted images plus high Cyst signal intensity on T2-weighted images Myxoma Myxoid liposarcoma Sarcoma Low to intermediate signal intensity on T1-weighted images plus low signal intensity on T2-weighted images Desmoid and other fibromatoses Pigmented villonodular synovitis Morton's neuroma Fibrolipohamartoma Giant cell tumor of tendon sheath Acute hematoma (few days) Old hematoma Xanthoma High-flow arteriovenous malformation Mineralized mass Scar tissue Amyloidosis Granuloma annulare High-grade malignancies

Intermediate signal intensity on T1-weighted images Neurogenic tumor plus high signal intensity on T2-weighted images Desmoid
Choroidal detachment is caused by the accumulation of fluid or blood in the potential suprachoroidal space [2,3]. Hemorrhagic choroidal detachment occurs after a contusion, penetrating ocular trauma, as in this case, or as a complication of ocular surgery. Vitreous hemorrhage and hyphema limit visualization of the fundus. Choroidal detachment significantly affects the prognosis of the injured eye [2]. Ultrasound, CT and MRI can all be performed to evaluate ocular injuries. CT is the best-suited modality for evaluation of a lacerated globe [1]. Hemorrhagic choroidal detachment appears as a mound-like area of high intensity on CT. MRI is also an excellent modality for evaluating patients with choroidal detachment. MRI shows choroidal hematoma as a focal, well-demarcated lenticular mass in the wall of the eyeball. The signal intensity of a hematoma depends on its age. Within the first 48 hours the hematoma is iso-intense to slightly hypointense to the normal vitreous body in T1-weighted MRI images. After 5 days choroidal hematoma appears hyperintense on T1-weighted images.

Hematoma usually continues to increase signal intensity on T1-weighted images and T2weighted images and becomes markedly hyperintense by two weeks on all MR sequences [2,3]. Serous choroidal effusion is the result of ocular hypotonia secondary to accidental perforation of the eye, as in this case, inflammatory disease such as uveitis or scleritis, ocular surgery or intensive glaucoma therapy. A choroidal effusion is seen as a cresentic or ringshaped lesion on CT and MRI [2,3]. It is not always possible to differentiate choroidal detachment from retinal detachment since the distinction of choroidal effusion from sub-retinal effusion is difficult [3,4].

The differential diagnoses of a white mass lesion in the ocular fundus of an adult include, metastatic carcinoma, amelanotic melanoma, lymphoma, astrocytoma, retinoblastoma, retinocytoma, endophthalmitis, panophthalmitis, and inflammatory diseases of the retina. Retinoblastoma in an adult creates a diagnostic dilemma owing to its low frequency. [7] The presence of Inflammation, vitreous hemorrhage, and cataract further augment difficulties in diagnosis. [4] Ultrasonography and a computed tomography scan may or may not reveal calcification, which is characteristic of retinoblastoma in children. Calcification is not an important finding in adult-onset retinoblastoma. [7] In our patient, calcification was present. Cases with diagnostic dilemma might undergo fine-needle aspiration cytology and immunohistochemistry with neuron-specific enolase. [8]

hypoxic-ischemic encephalopathy (HIE) MRI is the imaging modality of choice for the diagnosis and follow-up of infants with moderate-to-severe hypoxicischemic encephalopathy (HIE).[34, 35, 36] Conventional MRI sequences (T1w and T2w) provide information on the status of myelination and preexisting developmental defects of the brain. When performed after the first day (and particularly after day 4), conventional images may accurately demonstrate the injury pattern as area of hyperintensity. Conventional images are most helpful at

age 7-10 days, when the diffusion-weighted imaging (DWI) findings have pseudonormalized. Following a severe asphyxial event, a central pattern of injury is seen with injury to (1) the deep gray matter (ie, putamina, ventrolateral thalamus, hippocampi, dorsal brainstem, or lateral geniculate nucleus) and (2) the perirolandic cortex. These areas contain the highest concentration of N-methyl-D-aspartate (NMDA) receptors and are actively myelinating. Less severe or partial insult results in injury to the intervascular boundaries areas and is also called watershed injury. This type of lesions manifests in the infants as proximal extremity weakness or spasticity. Decreased signal in the posterior limb of the internal capsule (PLIC) on T1w images may be noted. The absence of normal signal (high intensity on T1w images) in the PLIC of infants older than 38 weeks' gestation is a strong predictor of abnormal motor outcomes in these infants.[37] DWI allows earlier identification of injury patterns in the first 24-48 hours. The MRI sequence identifies areas of edema and, hence, injured areas. DWI changes peak at 35 day and pseudonormalizes by the end of the first week. In neonates, DWI changes may underestimate the extent of injury, most likely because of the importance of apoptosis in the ultimate extent of neurological injury.[34] MRI is also a useful tool in the determination of prognosis. Studies indicate that infants with predominant injuries to the basal ganglia or thalamus (BGT) have an unfavorable neurological outcome when compared with infants with a white matter predominant pattern of injury. Abnormal signals in the PLIC have also been associated with poor neurological outcome. In a recent study, severe BGT lesions on early MRI (performed at a median of 10 d; range, 2-42 d) were strongly associated with motor impairment at 2 years. In addition, abnormal PLIC signal was also highly correlated with inability to walk

independently at 2 years, with a sensitivity of 0.92 and a specificity of 0.77.[38] MRI is also useful for follow-up. In any newly diagnosed case of cerebral palsy, MRI should be considered because it may help in establishing the cause. Note that the interpretation of MRI in infants requires considerable expertise. Magnetic resonance spectroscopy (MRS) allows for quantification of intracellular molecules. Proton MRS allows identification of cerebral lactate, which persist for weeks following a significant hypoxic-ischemic injury. Phosphorous MRS allows for real-time quantification of ATP, phosphorus creatinine, inorganic phosphorous, and intracellular pH levels.