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Writer's pictureJason Hewitt

Pathophysiology review: Neurological Pathologies

Neurological pathologies:


Cerebrovascular Accidnent (CVA/Stroke):

A CVA occurs when there is interruption of blood flow to an area of the brain. The resulting ischemia/infarction causes neurological disfunction in the systems associated with the affected areas of the brain. A CVA can occur in one of two possible forms: 1) Ischemic CVA, which accounts for 80% of CVAs that present to the ED, and 2) Hemorrhagic CVA, which make up the other 20%. In an ischemic CVA, a thrombus forms in one of the cerebral arteries. The clot can form as a result of vascular changes, just as we see in an MI, or it can be the result of an embolus (usually from one of the carotid arteries). The thrombus occludes the affected vessel, and cuts off blood flow to the tissue distal to it, resulting in cell death and neurological dysfunction. In a hemorrhagic CVA, a cerebral artery ruptures, usually at an area of weakening such as an aneurysm, due to elevated blood pressure over a prolonged period. The resulting drop in blood flow to the tissue perfuse by the affected artery causes ischemia. The hemorrhage itself causes elevation in intracranial pressure, and associated ischemia in the surrounding areas, as well as secondary injury to the tissue compressed against the skull. Typically hemorrhagic strokes have a higher mortality. Unfortunately, without the aid of imaging, it can be difficult to tell the two apart in the EMS setting, so both are treated essentially the same until arrival at the ED. Treatment in the hospital depends on several factors including: Time of symptom onset, Imaging results, Presence of known bleeding disorders, and availability of EVT. In the case of an ischemic CVA, the patient may be able to receive thrombolytic drugs to break apart the offending thrombus, or they may be able to receive Endovascular Therapy (EVT). Thrombolytics are generally possible up to 6 hours from time of onset, while EVT can be utilized up to 24 hours from onset.


Risk factors for CVA are important to catch during your past medical history. Look for history of:

  • Hypertension

  • Diabetes

  • High Cholesterol

  • Prior TIA

  • Coronary artery disease

  • Myocardial infarction

  • Atrial fibrillation

  • Pulmonary embolism

  • Obesity

  • Stimulant drug use


As Paramedics, our priority is rapid identification of CVA symptoms, and clear determination of time of onset or when the patient was last seen normal. This allows us to establish a window for appropriate treatment decisions. We typically use some variation of a F.A.S.T. Exam (Cincinnati Stoke screen), which assesses for:

  • Facial Droop

  • Bilateral Arms and legs for Grip/pedal strength and drift

  • Speech for slurring, inappropriate responses, or absence

  • Time of onset

Given the potential for airway compromise, we ensure patency is maintained, and support respirations as needed. A large bore IV should be placed in the AC Fossa as the hospital will need access to inject CT contrast dye. Pre-alert to the stroke team is a common practice, and you may need to bypass closer facilities to travel to the appropriate one. Follow local protocols.



TIA:

A TIA, or Transient Ischemic Attack, occurs when a blockage forms in a cerebral artery, causing interruption of blood flow to the tissue beyond. This is identical to the process that occurs during a CVA with one key difference; in this case the blockage is resolved in less than 24 hours, and does not leave neuro-deficits once cleared. From an EMS perspective, unless the symptoms have resolved prior to our arrival, we still treat it as though the patient is having a CVA. Even if we can determine that the patient has experienced a TIA, rather than an active CVA, we still need to transport them to the ED. A TIA is not generally an isolated event, and typically occurs a s precursor to a future CVA. Maintain the patient's ABCs, get a thorough history, and vitals including a blood sugar and 12-lead ECG.



Seizure:

Seizures occur when there is unregulated, sporadic, activity in the brain. Think of it like ventricular fibrillation for the central nervous system. The presentation of the seizure depends upon the region of the brain affected. Seizures themselves are classified as Generalized seizures, or Focal Seizures, based upon the degree of brain involvement and subsequent presentation.

Generalized seizures affect a large cerebral surface, and present with global motor and neurological impairment. They were once classified as Grand-mal or Petit-Mal seizures, however the terminology has since been update for accuracy. We now refer to them as Tonic-Clonic (Grand-mal) and Absence (Petit-mal) seizures.


In a Tonic-Clonic seizure, the patient has uncontrolled depolarization in the CNS, which affect both level of consciousness as well as motor control. These seizures present with the following pattern:

  • Aura: This is a sensation that the patient experiences immediately prior to having a seizure. It may be a tactile sensation, smell, sound, visual disturbance, etc.

  • Loss of consciousness

  • Tonic phase: Contraction of the skeletal muscles into a rigid state.

  • Clonic phase: Rapid alternation of the muscles between contracted and relaxed states.

  • Post-Ictal state: Post seizure period of altered level of awareness that gradually returns to a baseline state over several minutes.

  • Post-Seizure: Period of physical exhaustion.


In contrast to the dramatic presentation of the Tonic-Clonic seizure, is the Absence seizure. Absence seizures occur by the same mechanism as Tonic-Clonic seizures, with the exception being that they do not affect skeletal muscle tone. This is to say that the Absence seizure manifests solely with a period of unresponsiveness. The patient may appear to be alert, but does not respond to any external stimulus. Physical manifestations such as incontinence may also accompany this state. Absence seizures resolve with a post-ictal period, and post-seizure phase as well.


Focal Seizures are different from Generalized seizures in some ways, and similar in others. In a Simple Focal seizure, the patient remains alert and aware of the situation, all the while experiencing myoclonic contraction in an isolated area of the body. A Complex Focal seizure is the same thing with the exception that the patient experiences an altered level of awareness during the seizure. Focal Seizures can progress to Generalized seizures and should be taken just as seriously.




Status Epilepticus: ANY seizure lasting longer than 5 minutes in duration, or multiple seizures without a return to baseline cognition in between is considered a Status seizure. This is a medical emergency because, the longer a seizure takes to resolve, the harder it is to stop. Seizures that involve tonic-clonic activity can progress to rhabdomyolysis if not stopped rapidly. Perhaps more importantly though, a patient in active seizure is often apneic for periods of time during the seizure. Respiratory ad metabolic acidosis are a result, and there is potential for significant neurological damage if the seizure lasts too long.


Broadly speaking, seizures have 3 main causes:

  1. Structural causes: Structural abnormalities, tumours, and epilepsy, as well as traumatic injuries.

  2. Metabolic causes: DKA, Metabilic acidosis, Electrolyte imbalances.

  3. Febrile causes: Children < 5 years of age may suffer tonic-clonic seizures in the presence of a persistently high fever over several days.


Long-term management of seizures depends largely on the etiology. Patients with diagnosed epilepsy may be placed on anticonvulsive medications and might also have prescribed benzodiazapines to manage seizures at home. In the emergency setting, seizure management is targeted at management of the ABCs, and stopping the seizure activity. In EMS, we establish airway patency, provide supplemental oxygen, assist ventilations in apneic patients, establish IV access and provide benzodiazapines to stop the seizure. Once the seizure activity is stopped, we attempt to identify a cause and correct it if we can. If the patient has never had a seizure before, we should also consider 12-lead ECG acquisition, as cardiac causes may be present.



Syncope:

Syncope refers to a transient loss of consciousness and postural tone that results from a brief interruption of oxygen and glucose to the brain. Neurons require a continuous flow of glucose in order to function. Any disruption in this flow will cause immediate dysfunction. The loss of consciousness resolves within a few minutes and the patient spontaneously returns to baseline without any sort of post-ictal period. Syncope occurs as a result of one of three potential causes:

  • Orthostatic Syncope: Whenever a person changes position from lying or sitting, to a standing position, gravity causes a rapid pooling of venous blood toward the lower extremities. This causes a sudden drop in preload, and drop in blood pressure. Most of the time, we can compensate for this by increasing heart rate, and vaso-constriction, to ensure a dramatic drop does not occur. However, patients who are dehydrated, on beta-blockers or other cardiac medications, or lack the ability to compensate adequately, will experience syncope. This usually folows a patern of standing, dizziness, blurring or narrowing of the visual field, and LOC. These sensations that occur just prior to syncope are called a prodrome.

  • Reflex-mediated Syncope: Also often called Vaso-vagal Sycope, this occurs in situations where an individual bears down, experiences a stressful or fear-inducing event, or stands for a prolonged period of time. Stimulation of the vagus nerve causes vaso-dilation and a rapid drop in blood pressure. Again, the patient usually experiences a prodrome, and could tell they were going to lose cosciousness.

  • Cardiac Syncope: In the case of cardiac syncope, the patient's cerebral blood flow is interrupted due to dysfunction of the heart itself. In most cases, this occurs when the heart enters a suddent tachy-dysrhythmia or brady-dysrhythmia. Because cerebral perfusion is affected suddenly, there is almost always no prodrome associated with cardiac syncope. Upon regaining consciousness, the patient may complain of chest pain, dyspnea, or dizziness. Common offenders are: SVT, V-Tach, MI, A-Fib RVR, Long QT Syndrome, Brugada Syndrome, WPW, and Hypertrophic Cardiomyopathy.


Because of the overlap in symptoms between the potential causes of syncope, and the similarity to other conditions we need to be thorough in our assessment of these patients. ABCs should always be a priority, and oxygen should be considered in any patient with decreased SPO2. IV isotonic saline should be considered in treating hypotension. 12-lead ECG, BGL, Stroke exam, and orthostatic vitals should all be checked. In the setting of an unwitnessed syncope, we cannot rule out head injury or spinal injury. A rapid body survey may be indicated depending upon the location of the syncope and potential for secondary injuries.


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