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TRAUMATIC BRAIN INJURY

The GCS assesses motor, verbal and eye responses; while there is some variability in the categories, a GCS  from 13 to 15 is often designated as mild TBI, 8 or below is considered severe, and 9 to 12 is considered a moderate TBI (Jennett, 1998; Parikh et al., 2007).

There are two common conjec- tures regarding the etiology of mTBI. The first is that the frontal and an- terior cortices are vulnerable to neural contusion (Adams et al., 1980; Beaumont and Gennarelli, 2006; Brandstack et al., 2006; Levin et al., 1992). The second is that linear and rotational forces act on axon bun- dles, leading to axonal injury (Buki and Povlishock, 2006; Gennarelli et al., 1982; Meythaler et al., 2001; Povlishock et al., 1992). After initial injury, secondary mechanisms elicit biochemical, metabolic, and cellu- lar changes in the time frame of minutes, days and months (Giza and Hovda, 2001; Loane and Faden, 2010; Xiong et al., 1997).  

Although mTBI has long been considered a noncritical injury, serious short and long term effects have been documented.  

Traumatic brain injury (TBI) occurs when a traumatic event causes the brain to move rapidly within the skull, leading to damage. As illustrated in the poster (panel A), the event can be classified as either impact or non-impact, depending on whether the head makes direct contact with an object (impact) or encounters a non- impact force such as blast waves or rapid acceleration and deceleration (non-impact).

Currently, the severity of TBI is categorized based on the Glasgow Coma Scale (GCS), in which patients are scored on the basis of clinical symptoms, and the resulting overall score classifies their injury as mild (score: 13-15), moderate (score: 9-12) or severe (score: <9). 

Symptoms of mild to moderate TBI can include headaches, dizziness, nausea and amnesia; these injuries usually resolve within days to weeks of the insult. 

However, occasionally these injuries can result in long-term cognitive and behavioral deficits. Furthermore, there is evidence to suggest that moderate to severe TBI, and even repeat mild TBI, might be associated with increased risk of neurodegenerative diseases such as Alzheimer’s disease (Lye and Shores, 2000), chronic traumatic encephalopathy (McKee et al., 2009) and Parkinson’s disease (Hutson et al., 2011). 

Primary injury refers to the initial impact that causes the brain to be displaced within the skull. Secondary injuries gradually occur as a consequence of ongoing cellular events that cause further damage. Fluid percussion (FP), controlled cortical impact (CCI) and weight-drop injury are the most commonly used TBI models that can be modulated to generate injuries with characteristics of mild or severe TBI 

During the acute phase (≤1 hour) after TBI, there is a massive release of glutamate from presynaptic terminals, which disrupts ionic equilibrium on postsynaptic membranes. The amount of potassium (K+) released increases with injury severity, as measured by microdialysis (Katayama et al., 1990; Kawamata et al., 1992). 

In addition to rising [K+], calcium (Ca2+) accumulation is also commonly observed after TBI (Osteen et al., 2001). Accumulation of intracellular Ca2+ activates mitochondrial Ca2+ uptake. Ca2+ overloading of the mitochondria has been shown to induce oxidative stress and to impair mitochondrial function (Xiong et al., 1997; Peng and Jou, 2010).  

Increases in 45Ca2+ were seen as early as 6 hours after the initial injury, and a return to control levels has been observed between 4 days (Fineman et al., 1993) and 7 days (Deshpande et al., 2008) post-injury. Ca2+ accumulation corresponded with the presence of cognitive deficits, which were detected using the spatial memory task, the Morris water maze.  

PARKINSON

PERLAS DE PARKINSON

The  D1 dopamine receptor is predominantly expressed on the STIATONIGRAL NEURONS, while the D2 receptors are primarily found on the STRAITOPALLIDAL NEURONS.

Evidence suggests that in the striatum the D1 and D2 receptors have, respectively, an EXCITATORY ( STRIATONIGRAL) and INHIBITORY action( STRIATOPALIDO)

Activation of the D1 receptors appears to be important in mediating DYSTONIC MOVEMENTS,whereas activation of the D2 receptors may result in CHOREA.

The dopaminergic deafferentation produces an imbalance in the stratal activity, with HYPOACTIVITY OF THE STRAITONIGRAL PATHWAY, and HYPERACTIVITY OF THE STRIATOPALLIDAL PATHWAYS.

The final effect of Dopamine deficiency is poverty or slowness of movements( HYPOKINESIA)

DATOS PARA REPASO

• Aura ( del griego viento suave y apacible) no es una convulsion, es por si misma una crisis epiléptica focal ( parcial simple)
• Fase preictal( antes de la crisis), que incluye circunstancias previas al inicio de la crisis 
• Fase ictal ( durante la crisis) 
• Fase postictal ( después de la crisis), los síntomas o signos inmediatos o mediatos al terminar la crisis ( debilidad de un hemicuerpo - parálisis de Todd-, disfasia, confusion mental, cefalea, sueño)
• Fase interictal ( entre una crisis y otra)

Crisis focales discognitivas ( con impedimento de la conciencia) en las que existe una propagación de la descarga eléctrica que involucra al sistema limbico.

Conciencia se define como la capacidad del paciente para percatarse y responder a los estimulos del ambiente. La presencia de amnesia para el evento ictal es suficiente evidencia de alteracion de la conciencia para permitir un diagnostico de crisis focal discognitva.

Las crisis focales son la forma más común de epilepsia en los niños.

Las crisis parciales complejas ( focales con perdida conocimiento), anteriormente denominadas crisis del lòbulo temporal o psicomotoras, se encuentran entre los tipos de crisis más frecuentemente observadas, tanto en niños como en adultos.

Los automatismos son comportamientos repetitivos y estereotipados que no dejan ordinariamente ningún recuerdo. Estos son la marca distintiva de las crisis focales discognitivas ( parciales complejas) y ocurren en 50% a 75% de los casos, particularmente en niños mayorcitos y adolescentes.

Durante la crisis, la descarga epileptiforme puede extenderse del lóbulo temporal hacia toda la corteza desencadenando una convulsion tonicoclonica generalizada ( crisis secundariamente generalizada)

La mayoría de los niños que tienen crisis focales con discognitiva ( parcial compleja) tienen un EEG anormal caracterizado por ondas agudas o descargas de puntas en la región temporal anterior o en el lobulo frontal o puntas multifocales.

STOKE

http://stroke.ahajournals.org/content/early/2013/05/07/STR.0b013e318296aeca.full.pdf+html

Table 1. Definition of Stroke 
The term “stroke” should be broadly used to include all of the following: Definition of CNS infarction: CNS infarction is brain, spinal cord, or retinal 
cell death attributable to ischemia, based on
1. pathological, imaging, or other objective evidence of cerebral, spinal cord, 
or retinal focal ischemic injury in a defined vascular distribution; or 2. clinical evidence of cerebral, spinal cord, or retinal focal ischemic 
injury based on symptoms persisting ≥24 hours or until death, and other etiologies excluded. (Note: CNS infarction includes hemorrhagic infarctions, types I and II; see “Hemorrhagic Infarction.”) 

Definition of ischemic stroke: An episode of neurological dysfunction caused by focal cerebral, spinal, or retinal infarction. (Note: Evidence of CNS infarction is defined above.) 

Definition of silent CNS infarction: Imaging or neuropathological evidence of CNS infarction, without a history of acute neurological dysfunction attributable to the lesion. 

Definition of intracerebral hemorrhage: A focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma. 
(Note: Intracerebral hemorrhage includes parenchymal hemorrhages after CNS infarction, types I and II—see “Hemorrhagic Infarction.”) 

Definition of stroke caused by intracerebral hemorrhage: Rapidly developing clinical signs of neurological dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma. 

Definition of silent cerebral hemorrhage: A focal collection of chronic blood products within the brain parenchyma, subarachnoid space, or ventricular system on neuroimaging or neuropathological examination that is not caused by trauma and without a history of acute neurological dysfunction attributable to the lesion. 

Definition of subarachnoid hemorrhage: Bleeding into the subarachnoid space (the space between the arachnoid membrane and the pia mater of the brain or spinal cord). 

Definition of stroke caused by subarachnoid hemorrhage: Rapidly developing signs of neurological dysfunction and/or headache because of bleeding into the subarachnoid space (the space between the arachnoid membrane and the pia mater of the brain or spinal cord), which is not caused by trauma. 

Definition of stroke caused by cerebral venous thrombosis: Infarction or hemorrhage in the brain, spinal cord, or retina because of thrombosis of a cerebral venous structure. Symptoms or signs caused by reversible edema without infarction or hemorrhage do not qualify as stroke. 

Definition of stroke, not otherwise specified: An episode of acute neurological dysfunction presumed to be caused by ischemia or hemorrhage, persisting ≥24 hours or until death, but without sufficient evidence to be classified as one of the above. 

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Stroke is classically characterized as a neurological deficit attributed to an acute focal injury of the central nervous system (CNS) by a vascular cause, including cerebral infarction, intracerebral hemorrhage (ICH), and subarachnoid hemorrhage (SAH), and is a major cause of disability and death worldwide. 


The current World Health Organization definition of stroke (introduced in 1970 and still used) is “rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin.”  


In 2009, an expert committee of the AHA/ASA published a scientific statement defining TIA and recommending evaluation. The definition proposed was “transient ischemic attack (TIA): a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction.” 


Based on advances including modern brain imaging, the 24-hour inclusion criterion for cerebral infarction is inaccurate and misleading, because permanent injury can occur much sooner.  

However, the location and extent of infarction is one variable to consider when choosing treatment. 

The word “transient” indicates a lack of permanence.    

Modern brain imaging has shown that many patients in whom symptoms and signs of brain ischemia are clinically transient have evidence of brain infarction. If the ischemia caused death of the tissue, it is misleading to designate the ischemia as transient. Similarly, ischemia may produce symptoms and signs that are prolonged (and so qualify in older definitions as strokes), and yet no permanent brain infarction has occurred. 


Knowledge of neuroanatomy and vascular anatomy is important for the clinical diagnosis of stroke and transient CNS ischemia. Brain injuries attributable to vascular causes are nearly always focal, unless they lead to increases in intracranial pressure that cause global cerebral hypoperfusion, as in SAH, or massive infarcts and ICHs.  

During clinical diagnosis, 3 questions require an answer: (1) Is the process vascular or a stroke-like mimic? If a vascular process, then (2) where in the CNS is the abnormality, and which blood vessels supply that area? and (3) What is the disease mechanism (e.g., ischemia or hemorrhage)? 



Retinal infarction is a clinical diagnosis in a patient with acute painless visual loss, typically associated with ischemic whitening of the retina observed on funduscopic examination. A “cherry red spot” may be evident in the macula in patients with central retinal artery occlusion. Retinal infarction rarely requires additional testing to confirm the diagnosis, although occasionally fluorescein angiography is used in atypical cases. 

Radiographic Diagnosis    


Traditional ideas that a strict brain time window exists for acute stroke differ from modern imaging findings obtained by methods such as MRI diffusion-weighted imaging (DWI), which highlights tissue changes after several minutes to days after transient or permanent ischemic events.12,13 A recent Cochrane review of CT and MRI for the diagnosis of acute cerebral infarction within 12 hours of symptom onset showed that the pooled estimates for CT sensitivity and DWI MRI sensitivity were 0.39 and 0.99, respectively, using a clinical diagnosis as the reference standard.


Today, attention is focused on multisequence use of rapid MRI as a biomarker for acute identification of permanent tissue injury as well as viable tissue at risk, widely known as the penumbra.15 Multimodal magnetic resonance angiography, DWI, fluid-attenuated inversion recovery (FLAIR), and perfusion-weighted MRI are used to detect “mismatch,” which identifies the area of potentially reversible injury.  


The use of all of these imaging studies is based on the underlying hypothesis that if the blood supply is not restored, the penumbra will succumb to permanent injury eventually and result in a negative clinical outcome.  

Pathology   


The histopathological criteria for recognizing acute irreversible ischemic neuronal injury (necrosis) have been recognized for decades: An affected neuron loses its basophilic cytoplasm (the result of Nissl substance, or rough endoplasmic reticulum) and prominently nucleolated nucleus, which are replaced by a neuronal cell body showing brightly eosinophilic neuronal cytoplasm lacking identifiable substructure, and a pyknotic or collapsed nucleus; the tinctorial change in the cytoplasm may precede nuclear change (Figure 1).  

A, Subacute cerebral infarction involving left cerebral hemisphere (indicated by arrowheads) that had occurred ≈3 to 4 days before death. Note the pronounced cerebral edema with left-to-right shift of midline structures, including subfalcine herniation of the cingulate gyrus, and marked central diencephalic herniation. 

C, Old cystic cerebral infarcts (observed at autopsy) in 2 different patients. Brain at left shows appearance of left cerebral hemisphere immediately after calvarium has been removed. Arrowheads indicate a large cavity in the middle cerebral artery territory. Brain (coronal section) at right shows a large right MCA territory infarct (indicated by arrowheads) in a patient who had experienced stroke many years previously.  

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The timing of the neuroimaging in relation to the onset of ischemia may impact whether imaging evidence of stroke is seen, since signs of ischemia on noncontrast head CT are seen within the first few hours of CNS infarction in 31% to 60% of cases.45–48 Therefore, within the first 12 hours of an acute stroke, a tissue-based diagnosis of CNS infarction is not possible with the use of routine noncontrast head CT alone but could be if MRI were widely used. Because noncontrast head CT remains the most commonly used imaging modality in the acute setting,49 a patient may have a clear clinical vascular syndrome supporting a diagnosis of CNS infarction but not meet a tissue-based definition of CNS infarction if only CT is used. 

Although the duration of ischemia is important in both focal and global ischemia, focal ischemia is acutely treated with reperfusion strategies to improve flow in an artery. In distinct contrast, global ischemia is acutely treated by correcting the systemic disorder that is the underlying cause of hypo perfusion   


The evaluation of patients with focal and global ischemia also differs. Focal ischemia typically requires assessment of the cervical and cerebral arteries, investigation of a possible cardiac source of emboli, and evaluation of risk factors for atherosclerosis, whereas the evaluation of global ischemia is focused on identifying the underlying cause of hypo perfusion. 


Patients with focal ischemia present with neurological deficits that are localizable to a particular vascular distribution and rarely have a depressed level of consciousness.

However, patients with global ischemia    most commonly present with diffuse nonfocal neurological symptoms, particularly diminished consciousness. The prognosis also differs between focal and global ischemia, because mortality for focal ischemia is ≈12%,56 while for global ischemia >80% of patients do not survive hospitalization, with two thirds of the deaths attributable to neurological injury.

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The brain, spinal cord, and retina derive from neural tube tissue and therefore constitute the CNS, while the cranial and peripheral nerves derive from neural crest tissue.62 There are differences in the mechanisms of ischemia, treatment, and recovery between CNS and peripheral nervous system (PNS) ischemia that warrant limitation of the definition of infarction to the CNS.  


CNS ischemia, as previously described, results from stenosis or occlusion of both large vessels and small vessels attributable to local thrombosis or embolization from other vascular regions or from critical hypoperfusion in border-zone regions. PNS ischemia typically results from small-vessel occlusion of the vasa nervorum presenting as mononeuropathies, most commonly related to vasculitis or diabetes mellitus. 


For CNS ischemia, the treatment is focused on establishing reperfusion in the acute setting and then secondary prevention of ischemia. For PNS ischemia, treatments are focused on the underlying condition (ie, steroids for vasculitis or glucose control for diabetes mellitus), and acute reperfusion treatments are not available. The CNS and PNS also differ with respect to potential for recovery after ischemic injury. The PNS has a greater regenerative capacity than the CNS because of innate differences between the neurons and supportive cells in these locations, allowing for PNS axonal regeneration after injury.
 

REFLEJOS

El arco reflejo de estiramiento consta de un órgano capaz de reaccionar a la distensión ( huso muscular), un nervio periférico ( axón), la sinapsis de la médula espinal y las fibras musculares. Los impulsos descienden desde el cerebro a través de los fascículos largos ( neurona motora superior) y modulan el reflejo. Por regla, una interrupción en el arco reflejo básico ocasiona la pérdida de éste, en tanto que las presiones ejercidas sobre la raíz nerviosa misma pueden disminuir su intensidad ( hiporreflexia). La interrupción del control regulatorio de la moto-neurona superior sobre el reflejo finalmente lo tornara hiperactivo ( hiperreflexia)

REFLEJOS ANORMALES

En pacientes con papaplejía pueden producirse reflejos anormales en las extremidades inferiores. El signo de Babinski y el de Oppenheim son los reflejos anormales que indican una lesión de neurona motora superior.

Signo de Babinski

Produzca la reacción plantar haciendo pasar un instrumento ligeramente puntiagudo a través de la superficie del pie así como a través del calcaneo y el borde lateral de la porción anterior del pie. Normalmente, en una reacción negativa, los dedos representan una flexión plantar. Una reacción positiva ( signo de Babinski) ocurre cuando el dedo gordo se extiende conforme los demás dedos experimentan dorsiflexion. Este signo indica que una lesión de neurona motora superior -una afección del fasciculo corticoespínal. En lactantes, la presencia del signo de Babinski es normal mas que patológico. Sin embargo, debe desaparecer hacia los 12 a 18 meses de edad.

Signo de Oppenheim

Para producir el signo de Oppenheim, recorra su dedo a lo largo de la cresta de la tibia. Normalmente no debe haber reacción del todo, o el paciente debe quejarse de dolor cuando se le hace la prueba. En circunstancias anormales, la reacción es la misma que en la estimulación plantar, es decir, el dedo gordo se extiende conforme los dedos experimentan flexión plantar ( signo de Oppenheim). El signo de Oppenheim no es tan confiable como el signo de Babinski y debe utilizarse como una confirmación de un signo de Babinski positivo.

Las personas tetraplejicas presentan también reflejos anormales en las extremidades superiores e inferiores. Puede producirse el signo de Hoffman en la extremidad superior y, si esta presente, es un signo de lesión de la neurona motora superior.

Para buscar el signo de Hoffman, pellizque la uña del dedo medio del paciente. Normalmente no debe haber alguna reacción. La flexión de la falange terminal del pulgar y de la segunda y tercera falanges de otro dedo constituyen una reacción positiva.

LESIONES

La lesión del nervio mediano completa o compresión excesiva y crónica que afecta la motricidad del dedo pulgar, indice y parcialmente el dedo medio, disminución de fuerza o falta de esta, con el tiempo perderá la función ya que los músculos se atrofia por daño del nervio

La parálisis del nervio radial, también conocida como Mano caída, es una enfermedad donde la persona no puede extender su muñeca y esta cuelga flácidamente.