Neuro

• Epidural hematoma


  Hematoma covering a portion of the dura
• Subdural hematoma


  Bridging veins travel from the surface of the cerebral hemispheres through the subarachnoid space and the subdural space to empty with dural vessels into the superior sagittal sinus

  
• Brain floating freely in CSF


  Can move within the skull, but the venous sinuses are fixed
• Displacement of the brain in trauma

  Can tear the bridging veins at the point where they penetrate the dura
• Subdural hematoma in elderly patients

  • Bridging veins are stretched out and the brain has additional space for movement, hence the increased rate of subdural hematomas in these patients, even after relatively minor head trauma
• Subdural hematoma in infants


  • Bridging veins are thin-walled
• Subdural hematoma


  Most often becomes manifest within the first 48 hours after injury
• Subdural hematoma


  • Most common over the lateral aspects of the cerebral hemispheres and are bilateral in about 10% of cases
• Subdural hematoma

  • Neurologic signs commonly observed are attributable to the pressure exerted on the adjacent brain
• Subdural hematoma

  • There may be focal signs, but often the clinical manifestations are nonlocalizing and include headache and confusion
• Subdural hematoma


  • In time, there may be slowly progressive neurologic deterioration, but acute decompensation is rare
• Subarachnoid and intraparenchymal hemorrhages

  Most often occur concomitantly in the setting of brain trauma with superficial contusions and lacerations
• Spät-apoplexie (delayed posttraumatic hemorrhage)

  Syndrome of sudden, deep intracerebral hemorrhage that follows even minor head trauma by an interval of 1 to 2 weeks
• Sequelae of brain trauma

  • Posttraumatic hydrocephalus
  • Posttraumatic dementia and the punch-drunk syndrome (dementia pugilistica)
  • Posttraumatic epilepsy
  • Posttraumatic brain tumors (meningioma)
  • Posttraumatic infectious diseases
  • Posttraumatic psychiatric disorders
• Spinal cord injury


  Level of cord injury determines the extent of neurologic manifestations

  
• Spinal cord injury


  • Lesions involving the thoracic vertebrae or below can lead to paraplegia
  • Cervical lesions result in quadriplegia
  • Those above C-4 can, in addition, lead to respiratory compromise from paralysis of the diaphragm

  
• Spinal cord injury


  Segmental damage to the descending and ascending white matter tracts isolates the distal spinal cord from its cortical connections with the cerebrum and brainstem; this interruption, rather than the segmental gray matter damage that may occur at the level of the impact, causes the principal clinical deficits

  
• Factors that contribute to spinal cord injury

  • Traumatic tissue disruption
  • Vascular injury/ischemia
  • Excitotoxicity

  
• Spinal cord injury - Morphology

  • At the level of injury, the acute phase consists of hemorrhage, necrosis, and axonal swelling in the surrounding white matter
  • In time, the central necrotic lesion becomes cystic and gliotic; cord sections above and below the lesion show secondary ascending and descending wallerian degeneration, respectively, involving the long white matter tracts affected at the site of trauma

  
• Complete SCI injury


  No VOLUNATARY movemenet or sensation below the level of injury
• Incomplete SCI injury


  At least some voluntary movement or sensation below the level of injury
• Anterior Cord Syndrome


  • Damage to the corticospinal and spinothalamic tracts
  • Dorsal column function is intact
  • Loss of motor function and pain and temperature sensation
  • Vibration, position and touch are maintained

  
• Cauda Equina Syndrome


  • Peripheral nerve injury to lumbar, sacral and coccygeal nerve roots
  • Variable motor and sensory loss in lower extremities
  • Sciatica
  • Bowel and bladder dysfunction
  • Saddle anaesthesia

  
• Degenerative diseases


  Diseases of gray matter with progressive loss of neurons
• Degenerative diseases


  • The pattern of neuronal loss is selective
  • The diseases arise without any clear inciting event in patients without previous neurologic deficits
• Anatomic regions of the CNS primarily affected by degenerative diseases


  • Cerebral cortex
  • Subcortical areas
• Protein aggregates in neurodegenerative disorders


  • They are resistant to normal cellular mechanisms of degradation through the ubiquitin-proteasome system
  • They are generally cytotoxic
• Degenerative diseases affecting the cerebral cortex


  • Alzheimer Disease
  • Frontotemporal Dementias
  • Frontotemporal Dementia with Parkinsonism Linked to Chromosome 17 (FTD(P)-17)
  • Pick Disease
  • Progressive Supranuclear Palsy (PSP)
  • Corticobasal Degeneration (CBD)
  • Frontotemporal Dementias Without Tau Pathology
  • Vascular Dementia

  
• Alzheimer disease


  • The major cortical degenerative disease
  • Its principal clinical manifestation is dementia
• Dementia


  Progressive loss of cognitive function independent of the state of attention
• Other causes of dementia


  • Frontotemporal dementia
  • Vascular disease (multi-infarct dementia)
  • Dementia with Lewy bodies (Parkinson disease)
  • Creutzfeldt-Jakob disease
  • Neurosyphilis
• Dementia is not part of normal aging and always represents a pathologic process
• Alzheimer disease


  • The disease usually becomes clinically apparent as insidious impairment of higher intellectual function, with alterations in mood and behavior
  • Later, progressive disorientation, memory loss, and aphasia indicate severe cortical dysfunction
  • Eventually, in 5 to 10 years, the patient becomes profoundly disabled, mute, and immobile

  
• Patients rarely become symptomatic before 50 years of age, but the incidence of the disease rises with age
• Most cases of Alzheimer disease are sporadic, although at least 5% to 10% of cases are familial
• Although pathologic examination of brain tissue remains necessary for the definitive diagnosis of Alzheimer disease, the combination of clinical assessment and modern radiologic methods allows accurate diagnosis in 80% to 90% of cases

  
• Gross morphology of Alzheimer disease


  • Cortical atrophy with widening of the cerebral sulci that is most pronounced in the frontal, temporal, and parietal lobes
  • Compensatory ventricular enlargement (hydrocephalus ex vacuo)

  
• Microscopic morphology of Alzheimer disease


  • Neuritic (senile) plaques
  • Neurofibrillary tangles
  • Cerebral amyloid angiopathy
• Neuritic plaques


  Focal, spherical collections of dilated, tortuous, silver-staining neuritic processes (dystrophic neurites) often around a central amyloid core, which may be surrounded by clear halo
• Neurofibrillary tangles


  Bundles of filaments in the cytoplasm of the neurons that displace or encircle the nucleus