Forensic Medicine

Tuesday, September 1, 2015

Neuroradiology

         An intra-axial abnormality arises from the brain parenchyma. An extra-axial lesion is one that arises outside of the brain substance and may be pial, dural, subdural, epidural, or intraventricular in origin. The most common extra-axial mass is a meningioma. In adults, the most common solitary intra-axial masses are primary brain tumors and metastatic disease. An intra-axial mass lesion expands the brain, results in gyral swelling, and/or results in effacement of the cerebral sulci. Imaging features that identify a mass as extra-axial include inward buckling of the gray and white matter, the presence of a cleft (which may be CSF, dura, and/or small vessels) separating the extra-axial mass from the brain, and the presence of remodeling of the adjacent osseous calvarium.

·         It is important to remember that the availability and speed of CT, as well as its high sensitivity in detecting treatable lesions, makes it the imaging modality of choice for the initial assessment of trauma patients with head injury! MRI is more sensitive in distinguishing between the different ages of blood (hyperacute, acute, subacute, and chronic), in detecting shear injury (diffuse axonal injury), and in detecting injury in the posterior fossa and the undersurfaces of the frontal and temporal lobes. MRI is less sensitive than CT in detecting subarachnoid hemorrhage, intracranial air, and fractures. In addition, there are logistic difficulties in performing MRI on trauma patients. MRI times are significantly longer, performing MRI in patients on ventilators and other monitoring devices can be very cumbersome, and the location of most MRI scanners is outside of the emergency department.

·         The corpus callosum is the largest white matter tract, and it connects the two cerebral hemispheres in the midline. The most common tumors that affect the corpus callosum are the GBM and lymphoma. The extension of a neoplasm from one hemisphere to the other via the corpus callosum produces the so-called "butterfly" pattern. Other non-neoplastic white matter diseases that commonly involve the corpus callosum include demyelinating disease (especially multiple sclerosis) and trauma (diffuse axonal injury).

·         The clinical manifestations of pineal region masses are dependent on their size and location near critical anatomic structures: the aqueduct of Sylvius, the tectal plate, and the vein of Galen/internal cerebral veins. Pineal region masses may cause paresis of upward gaze (Parinaud's syndrome) due to compression of the tectal plate or obstructive hydrocephalus due to compression of the aqueduct. Pineal region tumors are categorized into those arising from germ cell origin (60%) and those from pineal cell origin. The majority of these tumors arise from germ cells, are seen in males, and are germinomas. Intrinsic pineal cell tumors (pineocytoma and pineoblastomas) are seen in male and female patients equally. CSF seeding is not uncommon. Because pineal tumors are commonly hypercellular, they appear hyperdense on unenhanced CT, and they are intermediate in signal intensity on T1- and T2-weighted MR images.

·         Imaging Manifestations of Ischemic Stroke in the Acute Stage: Commonly, in the acute setting, a CT of the head may be normal! The earliest signs (within 6 hours) of an acute infarct on CT are loss of the gray-white differentiation with obscuration of the lateral lentiform nucleus. There may be a high density noted in the proximal middle cerebral artery, representing acute thrombus or calcified embolus. This is referred to as the "hyperdense artery sign". Within 12-24 hours, there will be low density in the appropriate vascular distribution, with increasing mass effect. Mass effect peaks between 3-5 days. Findings of acute ischemia are detected earlier on MRI. With the use of diffusion-weighted imaging, acute ischemic changes can be seen within minutes of onset of the ictus. High signal intensity is noted within the involved vascular territory on T2-weighted images, with characteristic restricted diffusion (also hyperintense) on diffusion-weighted images. Swelling of the involved cortex and arterial enhancement are noted early in the time course.

·         Amyloid angiopathy results from deposition of amyloid in the media and adventitia of small and medium-sized vessels of the superficial layers of the cortex and leptomeninges. Amyloid deposition increases with age. Pathologically, there is loss of elasticity and increased fragility of the vessels that cause hemorrhages that are usually lobar and most often in the frontal and parietal lobes. These parenchymal hemorrhages may be associated with subdural and subarachnoid hemorrhage. The usual course is multiple hemorrhagic incidents spaced over time.

·         SPLIT NOTOCHORD SYNDROMES: Persistent midline adhesions between endoderm and ectoderm can result in splitting of the notochord. With this split, paired hemicords (diastematomyelia) may result. Persistent endodermal-ectodermal adhesions/communications may produce dorsal enteric fistulas and neuroenteric cysts.
1.       Diastematomyelia predominantly occurs in female patients. In 85% of cases, the split occurs between T9 and S1. The cord is split by a fibrous, osseous, or osteocartilaginous septum, and the hemicords may or may not share a dural sac. Associated neurologic and orthopedic anomalies are common.
2.       Dorsal enteric fistulas are very rare and extend from the mesenteric surface of the gut through the prevertebral tissues, vertebrae, and spinal cord to the dorsal skin surface.
3.       Neuroenteric cysts are most often intradural, extramedullary cystic masses in the thoracic region. Vertebral anomalies are seen in fewer than half of the cases.

·         Baastrup's disease: Apparent enlargement and flattening of the spinous process, particularly in the lumbar spine, which may be secondary to excessive lordosis resulting in close contact of the spinous processes and subsequent sclerosis of the spinous processes and degeneration of the interspinous ligaments. This may cause pain and tenderness and is seen well on radiographs or MRI

·         FRACTURES A/W CERVICAL SPINE INJURY:
1.       Hyperflexion may cause compression fractures, flexion-teardrop fractures, and spinous process fractures. When associated with posterior ligamentous injury, subluxations and bilateral facet dislocations may result. When hyperflexion occurs with rotation, this mechanism may result in unilateral facet dislocations.
2.       Hyperextension injuries include extension-teardrop fractures, fractures of the atlas, "hangman's" fractures (through the pars interarticularis of C2) (see Fig. 35-2), laminar fractures, and fracture/dislocations. When hyperextension occurs with rotation, pillar fractures and pedicle-laminar separation may result.
3.       Vertical compression or axial loading injuries (when force is transmitted through the top of the skull through the occipital condyles and vertebral column) result in burst fractures of the vertebral bodies. In the cervical spine, burst fracture of the atlas (C1) is most common.
4.       Lateral flexion usually occurs in conjunction with vertical compression. Isolated lateral flexion is the typical mechanism of injury resulting in isolated fractures of the uncovertebral joint of the cervical spine.
5.       Some injuries, such as odontoid fractures and atlanto-occipital dislocations, result from complex, often combined forces.

·         SPINAL VASCULAR MALFORMATIONS:
1.       Dural arteriovenous malformations are the most common of the spinal vascular anomalies seen in adults. They typically affect middle-aged and older men, who present with chronic, progressive motor and sensory deficits, usually in the lower extremities. Bowel, bladder, and sexual dysfunction also often occur. These are acquired lesions, most often occurring in the lower thoracic and upper lumbar spine. Arterial supply is from the dural arteries. MRI is notable for diffuse enlargement and signal abnormality within the cord, generally involving the conus. Large vessels, representing dilated veins, are seen within the thecal sac. Enhancement may be present within the cord. The diagnosis is confirmed with spinal angiography. Treatment consists of embolization and/or surgery.
2.       Arteriovenous malformations are seen in younger patients (often teenagers) and often present acutely secondary to intramedullary and/or subarachnoid hemorrhage. The arteriovenous malformation nidus is located within or on the surface of the cord and is supplied by the anterior or posterior spinal arteries. In the juvenile variant, the nidus also involves the vertebral column.
3.       Arteriovenous fistulas are relatively uncommon. They are direct intradural fistulous connections from the anterior or posterior spinal arteries to the pial veins. These lesions typically occur in the thoracic and lumbar regions. Patients with these lesions may have a slowly progressive myelopathy or radiculopathy or may present with subarachnoid hemorrhage. These lesions usually present in the second to fourth decades.
4.       Cavernomas may occur anywhere in the spinal cord. They may present at any age, chronically or acutely (secondary to hemorrhage). Back pain is often reported. On imaging studies, they are often well-demarcated intramedullary lesions with a surrounding hemosiderin ring (hypointense on T2-weighted MR images). Surrounding signal abnormality due to edema or gliosis may be present, and these lesions may be calcified. Symptomatic lesions are treated with surgical excision.

·         SAS/leptomeningeal tumor is characterized by tiny nodules of tumor implanted on the surface of the brain and/or spinal cord. There is "sugar-coating" of the subarachnoid spaces. T1-weighted MRI with contrast enhancement is best at demonstrating this nodular enhancement, particularly in the basilar cisterns, over the cerebral convexities, and along the cranial nerves. Communicating hydrocephalus may result from obstruction of the arachnoid villi. Many primary CNS tumors seed the subarachnoid spaces (GBM, oligodendroglioma, ependymoma). Metastatic systemic tumors that commonly spread to the CSF/leptomeninges include breast and lung carcinoma, melanoma, and hematologic malignancies (lymphoma and leukemia).

·         On magnetic resonance imaging (MRI), the demyelinating lesions of MS are ovoid and hyperintense (bright) on T2-weighted images and occur predominantly in the white matter, especially in the periventricular location (usually perpendicular to the ventricular surface)

·         ring-enhancing lesion in the brain: The following disease processes can have an imaging presentation identical to brain abscess: metastatic disease, primary CNS glioma, resolving hematoma, and demyelinating disease. Interpreting the radiologic findings in conjunction with the clinical history is usually very helpful in differentiating among these possible etiologies.

·         Amyloid angiopathy results from deposition of amyloid in the media and adventitia of small and medium-sized vessels of the superficial layers of the cortex and leptomeninges. Amyloid deposition increases with age. Pathologically, there is loss of elasticity and increased fragility of the vessels that cause hemorrhages that are usually lobar and most often in the frontal and parietal lobes. These parenchymal hemorrhages may be associated with subdural and subarachnoid hemorrhage. The usual course is multiple hemorrhagic incidents spaced over time.

·          CLASSIFICATION OF TUMORS AND OTHER LESIONS WITHIN THE SPINAL CANAL
1.       Extradural (outside the thecal sac): disc pathology, metastasis, epidural abscess, hematoma, bone abnormality
2.       Intradural-extramedullary (inside the thecal sac but outside the cord): nerve sheath tumor (neurofibroma, schwannoma), meningioma, metastases, lipoma, arachnoid cyst
3.       Intramedullary (inside the cord): tumors (astrocytoma, ependymoma, hemangioblastoma), multiple sclerosis, cord infarct, arteriovenous malformation, syrinx

·         Extramucosal spaces of the head and neck:
Lateral to the pharyngeal airway are the parapharyngeal space (PPS), masticator space (MS), parotid space (PS), and carotid space (CS). Posterior to the pharyngeal airway are the retropharyngeal space (RPS) and the perivertebral space (PVS). The PPS is the central, primarily fat-containing space around which the other extramucosal spaces are located. The PPS contains fat, lymphatics, nerves, and minor salivary gland tissue. The MS contains the muscles of mastication (lateral and medial pterygoid and masseter and temporalis muscles), the ascending ramus of the mandible, and the V3 branch of the trigeminal nerve. The PS includes the parotid gland, facial nerve, retromandibular vein, external carotid branches, and intraparotid lymph nodes. The CS includes the internal carotid artery, internal jugular vein, cranial nerves IX through XII, sympathetic plexus, and lymph nodes of the deep cervical chain. The RPS includes predominately fat and lymph nodes. The PVS includes the longus colli/capitis muscle complex, paraspinal musculature, vertebral body, posterior triangle of the neck, neurovascular structures within the spinal canal, and brachial plexus. The transverse process of the vertebral bodies further divide this space into the prevertebral portion anteriorly and the paraspinal portion posteriorly.
The PPS is the central, primarily fat-containing space that is surrounded by the MS anteriorly, CS posteriorly, PS laterally, and pharyngeal mucosal space medially. Deviation of the fat in the PPS can help localize large masses to one of these four spaces. Large MS lesions will deviate the PPS fat posteromedially, a mass in the PS will deviate it medially, a CS mass will deviate the PPS fat anteriorly, and submucosal extension of a pharyngeal mucosal mass will deviate the fat medially.

·         NECK LESIONS
  1. Neck lesions above the hyoid bone should be studied first with MRI. Pathologic conditions of the neck below the hyoid bone should be primarily imaged with CT scanning.
  2. The most common cause of a cystic neck mass in an adult is metastatic adenopathy.

·         The parotid is drained by Stensen's duct, which courses from the parotid gland and passes over the masseter muscle to insert into the cheek at the level of the second maxillary molar. The submandibular gland is drained by Wharton's duct, which drains on either side of the frenulum in the floor of the mouth. The sublingual glands consist of 12-18 small, paired glands located in the sublingual space in the floor of the mouth. The sublingual glands have many draining ducts, known as the ducts of Rivinus, which drain into the floor of the mouth. If there is a dominant sublingual duct opening into Wharton's duct, it is called the duct of Bartholin.

·         There is nothing specific about the appearance of an intrathyroidal mass (such as calcification, low attenuation, or hemorrhage) that distinguishes a benign nodule from a malignant nodule

·         ON Meningiomas occur in middle-aged adults, whereas optic nerve gliomas occur in children (mean age, 8-9 years). Meningiomas straighten the optic nerve because they arise from the surrounding dura of the optic nerve sheath complex, whereas gliomas kink the nerve as the tumor arises from the nerve itself. With meningiomas the mass can be separated from the optic nerve. Both can occur in children with neurofibromatosis, but optic nerve gliomas are the most common.

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