Module 8.1 - CNS Disorders Flashcards
1
Q
What is and what are the symptoms associated with a closed head injury?
A
- More common and involves the head striking a hard surface, a rapidly moving object striking the head or blast waves.
- The dura mater is intact and brain tissues are not exposed to the environment
- Blunt trauma can result in both focal brain and diffuse axonal injuries
- May be evidenced by immediate (generally no more than 5 minutes) loss of consciousness (LOC), loss of reflexes (fall to ground), transient cessation of respiration,briefperiod of bradycardia and decreased in blood pressure
- Increased cerebrospinal fluid (CSF) pressure and electrocardiogram (ECG) and electroencephalogram (EEG) changes occur on impact.
- Evaluation based on results of health history, LOC according to GCS, outcomes of imaging studies (CT or MRI) and assessment of vital parameters (ICP and EEG)
2
Q
What are the goals of treatment for patients with closed head injuries?
A
Treatment is directed at controlled ICP, neuroprotection and managing symptoms
3
Q
What is a contusion?
A
- A head injury produced by compression of the skull at the point of impact or, from blood leaking from an injured vessel.
- Injury may be coup (injury at site of injury) or contre-coup (injury from brain rebounding and hitting opposite side of skull) or both
4
Q
How is the severity of a contusion determined?
A
- Severity varies with the amount of energy transmitted by the skull to underlying brain tissue
- The smaller the area of impact, the more severe the injury because of the concentration of the force.
- Brain edema forms around and in damaged neural tissues, contributing to increasing intracranial pressure (ICP).
- Multiple hemorrhages, edema, infarction and necrosis can occur within the contused areas.
- Tissue has a pulpy quality
- Maximal effects of these injuries peak 18-36 hours after severe head injury
5
Q
What is an epidural hematoma?
A
- Occurs when there is bleeding between the dura mater and the skull
- An artery is the source of bleeding in 85% of epidural hematomas
- Usually accompanied by a skull fracture
6
Q
What is the most common site for an epidural hematoma?
A
- The temporal fossa is the MOST COMMON SITE of an epidural hematoma caused by injury to the middle meningeal artery or vein
- Individuals with a temporal epidural hematoma will suffer LOC immediately and become lucid within a few minutes
7
Q
What are the subjective/physical exam findings associated with an epidural hematoma?
A
As hematoma accumulates, patient will complain of:
- Headache- increasing in severity
- Vomiting
- Drowsiness
- Confusion
- Seizure
- Hemiparesis may develop
Temporal lobe herniation can occur with decreasing LOC, ipsilateral pupillary dilatation and contralateral hemiparesis
8
Q
How do you diagnose an epidural hematoma and how do you treat it?
A
- CT or MRI usually needed to diagnose epidural hematoma
- Medical emergency requiring surgical evacuation of hematoma
Prognosis good if treatment initiated prior to bilateral pupillary dilation occurs
9
Q
What is a subdural hematoma?
A
- Bleeding between the dura mater and the brain
- Occurs in 10-20% of TBI
- Acute subdural hematomas occur RAPIDLY, usually within hours
- Commonly located at the top of the skull (at the cerebral convexities)
- As ICP increases, the bleeding veins are compressed (self-limiting)
- Cerebral compression and displacement of brain tissue causes temporal lobe herniation if not treated
10
Q
What are the symptoms associated with a subdural hematoma?
A
- Headache
- Drowsiness
- Restlessness or agitation
- Slowed cognition and confusion
- Symptoms worsen over time and progress to LOC, respiratory pattern changes, and pupillary dilation
- Homonymous hemianopia (defective vision in either the right or the left field), dysconjugate gaze, and gaze palsies may occur.
11
Q
What is a subacute subdural hematoma?
A
- Develop more slowly, often over 48 hours to a few weeks
- Occur more often in older adults and those that abuse alcohol due to brain atrophy with a subsequent increase in the size of the extradural space
- These subdural hematomas act like expanding masses, increasing ICP that eventually compresses the bleeding vessels
- Brain herniation can result
12
Q
What is a chronic subdural hematoma?
A
- A subdural hematoma that develops over weeks to months
- Existing subdural space contains the liquefied clot from an acute bleed and/or accumulation of blood from a leaking vein
- A vascular membrane forms around the hematoma in approx. 2 weeks
- 80% will have chronic headaches and tenderness over hematoma on palpation
13
Q
What are the symptoms associated with a chronic subdural hematoma and what is the treatment?
A
Symptoms:
- Confusion
- Memory loss
- Coma
- Difficulty speaking or swallowing
- Weakness with difficulty walking
- Loss of sensation
- Seizures
Require a craniotomy to evacuate gelatinous blood and to prevent brain herniation
14
Q
What is an intracerebral hematoma?
A
- Occurs when there is bleeding within the brain
- Occur in 2-3% of head injuries, may be single or multiple and are associated with contusions
- MOST commonly located in the frontal and temporal lobes
- Penetrating or shearing forces traumatize small blood vessels
15
Q
What are the signs/symptoms associated with an intracerebral hematoma?
A
This hematoma acts as an expanding mass, increasing ICP, compressing brain tissues causing edema and ischemia leading to:
- Decreased LOC, coma or confusional state from other injuries can make the cause of this increasing unresponsiveness difficult to detect
- Contralateral hemiplegia may occur and as ICP rises, temporal lobe herniation may appear
Delayed intracerebral hematomas may appear 3-10 days after head injury
16
Q
How do you diagnose an intracerebral hematoma and how do you treat it?
A
- History and physical exam help to establish diagnosis
- CT/MRI and cerebral angiography confirm diagnosis
- Treatment is directed at reducing ICP to maintain cerebral perfusion pressure and allowing the hematoma to reabsorb slowly
17
Q
What are 4 different mechanisms of spinal cord injury?
A
- Hyperextension – Causes spinal cord to stretch (Ex: rear-end collisions, fall onto face, forehead or chin)
- Hyperflexion – greatest stress occurs at C5-6, causing bilateral facet dislocation
- Compression – Vertebral body is compressed and/or shattered, resulting in ‘burst’ fracture and bone fragments may become embedded into spinal cord (Ex: diving accidents or falls, when patient lands on their feet or buttocks)
- Whiplash – sudden hyperextension of the spine that stretches the ligaments as a result of the force of the lower body moving forward and the backward and downward movement of the head.
18
Q
Describe the anatomy of the spinal cord
A
A. 33 vertebrae total
- Cervical spine (C1-C7)
Highly flexible, small in diameter
Easy to fracture secondary to above
- Thoracic spine (T1 – T 12)
Articulates with ribs
Not a common site for fracture due to its stability with ribs
- Lumbar spine (L1-L5)
Highly mobile, large in diameter
Requires greater amount of force to fracture
- Sacral spine (S1-S5)
- Coccygeal vertebrae (3-5 coccyges)
B. Spinal Cord
- Gray matter
- White matter
- Meningeal layer (pia mater, arachnoid and dura mater)
19
Q
What are the 8 steps to conduct a physical assessment on a patient with a spinal cord injury?
A
1. Assess for airway, breathing and circulation and life-threatening injuries first
2. Assess respiratory ability: pulmonary complications main cause of early death in acute quadriplegia
- Chest excursion
- Use of intercostal muscles or diaphragm to breath
- Cervical cord injury at, or above, C3 results in respiratory arrest.
- Edema from upper cervical spine injury is considered life threatening secondary to breathing difficulty from impairment of diaphragm functioning.
- C5-C6 injuries spare the diaphragm, and diaphragmatic breathing can occur
- T1-L2 lesions can cause loss of intercostal muscle use
3. Assess need for Intubation if necessary
- Jaw thrust maneuver only
- Apnea
- Breathing difficulty
- Diaphragmatic fatigue exists
4. Monitor ABGs closely
5. Monitor for pneumonia, pulmonary edema and pulmonary emboli.
6. Motor assessment:
- Perform motor exam and grade strength on a 5 point scale
- Complete lesion: patient lacks sensory function, proprioception, and voluntary motor activity below level of injury; Worse prognosis for recovering neurologic function
- Incomplete lesion: parts of the spinal cord at the level of the lesion are intact; sacral sparing occurs; note sensory perception and voluntary contraction of the anus around the examiners finger
7. Assess Sensory function:
- Begin at the area of no feeling and proceed to the area of feeling
- Assess response to pain:
- Great toe L4
- Back of leg S1-S3
- Perianal area: S4-S5
- Umbilicus T10
- Nipple line T4
- Ring and little fingers C8
- Middle finger C7
- Thumb C6
- Top of shoulder C4
- If the patient is unable to feel pain the lesion is at or above the level spinal nerve level indicated above
8. Evaluate the patients back:
- Log roll patient- needs to be a coordinated maneuver
- Maintain in-line spinal stabilization
- Gently palpate spin for pain, tenderness, or gaps between spinous processes
- Observe for entrance or exit wounds, impaled objects or other injuries.
20
Q
What are signs of C2-C3 spinal cord injury?
A
- Respirator paralysis (breathing center C3)
- Phrenic nerves exit C3-C5
- Flaccid paralysis
- Areflexia (DTRs)
- Loss of sensation below mandible
21
Q
What are signs of C5-C6 spinal cord injury?
A
- Diaphragmatic breathing
- Paralysis of intercostal and abdominal muscles
- Quadriplegia
- Anesthesia below the clavicle and the ulnar half of the arm
- Areflexia (with possible exception of biceps reflex)
- Fecal and urinary retention
- Priapism (spontaneous erection)
22
Q
What are signs of T12-L1 spinal cord injury?
A
- Paraplegia
- Anesthesia in the legs
- Areflexia in the legs
- Fecal and urinary retention
- Priapism
23
Q
What are signs of L1-L5 spinal cord injury?
A
- Flaccid paralysis to partial flaccid paralysis
- Abdominal and cremasteric reflexes present
- Ankle and plantar reflexes absent
24
Q
What is a primary spinal cord injury?
A
- Occurs with the initial mechanical trauma and immediate tissue destruction from shearing, compression, or penetration
- Can also occur if the injured spine is NOT adequately immobilized immediately following the injury
- Can also occur in the absence of vertebral fracture or dislocation from longitudinal stretching of the cord with or without flexion or extension of the vertebral column or both.
- The stretching causes altered axon transport, edema, myelin degeneration and retrograde degeneration
25
What is a secondary spinal cord injury?
* **A pathophysiologic cascade of vascular, cellular and biochemical events that begin within a few minutes after injury and continues for a few weeks**
* Edema, ischemia, excitotoxicity (excessive stimulation, oxidative dame, and activation of necrotic and apoptotic cell death )
* Microscopic hemorrhages appear in the central gray matter and pia-arachnoid, increasing in size until the entire gray matter is hemorrhagic and necrotic
* Edema in the white matter occurs impairing the microcirculation of the cord
* **Hemorrhages** **and** **edema** **are followed by loss of autoregulation and reduced vascular perfusion and development of ischemic areas, which are maximal at the level of injury and two (2) cord segments above and below it.**
* Impaired perfusion is aggravated by systemic responses, including neurogenic or hemorrhagic shock and dysrhythmias
* **In the cervical region, cord swelling may be life-threatening**
* Diaphragm function may be impaired because of phrenic nerves which exit at C3 to C5.
* Cardiovascular and respiratory functions mediated by medulla oblongata may be lost.
26
What are the 4 types of vertebral injuries?
1. **Simple fracture:** a single break usually affecting transverse or spinous processes
2. **Compressed (wedged) fracture:** a vertebral body compressed anteriorly
3. **Comminuted (burst) fracture:** vertebral body shattered into several fragments
4. **Dislocation**
27
What is spinal shock?
Shock that develops immediately after spinal cord injury due to loss of continuous tonic discharge from the brain or brainstem and inhibition of suprasegmental impulses caused by cord hemorrhage, edema or anatomic transection
28
What are some characteristics of spinal shock?
* **_ALL motor, sensory, reflex and autonomic functions CEASE_ below any transected area and may cease below concussive, contused compressed or ischemic areas.**
* **There is flaccid paralysis,** **absence** **of sensation, loss of bladder and rectal tone/control, transient drop in blood pressure and poor venous circulation.**
* Condition also results in ***disturbed thermal control due to damage of the sympathetic nervous system***
* Hypothalamus cannot regulate body heat through vasoconstriction and increased metabolism; therefore, the patient assumes the temperature of the air (Poikilothermia)
* Spinal shock lasts 7-20 days usually with a range of a few days to 3 months
* **Terminates with the reappearance of reflex activity, hyperreflexia, spasticity and reflex emptying of the bladder.**
29
What is and what causes neurogenic shock?
* Occurs with **cervical or upper thoracic cord injury _ABOVE T6_**
* May be seen in addition to spinal shock
* **Caused by the absence of sympathetic activity through loss of supraspinal control and unopposed parasympathetic tone mediated by the intact vagus nerve**
* May last up to 5 weeks after injury
30
What are the symptoms associated with neurogenic shock?
**Symptoms include:**
1. Vasodilation
2. Hypotension
3. Bradycardia
4. Hypothermia (failure of body temperature regulation)\*\*\*due to sustained sympathetic nervous system damage
* Maybe complicated by hypovolemic or cardiogenic shock if there is concurrent heart failure or blood loss
* **Continued loss of motor and sensory function depends on** **extent** **and level of injury**
* Paraplegia: paralysis of lower half of body with both legs involved
* Quadriplegia: paralysis involving all four extremities
* Complete quadriplegia: injury above C6; all upper extremity function is lost
* Incomplete quadriplegia: function at or above C6 is preserved; leaving the shoulder, upper arm and some forearm muscle control intact
31
What is/causes autonomic hyperreflexia (dysreflexia)?
**IS:**
* A sudden life threatening **massive reflex sympathetic** discharge associated with spinal cord injury at level **T6 or above where descending inhibition is blocks**
**CAUSE:**
1. Sensory receptors below the level of the cord lesion are stimulated
2. Intact autonomic nervous system reflexively responds with an arteriolar spasm that increases blood pressure
3. Baroreceptors in cerebral vessels, carotid sinus and aorta sense the HTN and stimulate the parasympathetic system
4. HR decreases, but the visceral and peripheral vessels do not dilate because efferent impulses cannot pass through the cord.
5. **MOST** **COMMON cause is a distended bladder or rectum; however, any sensory stimulation (skin or pain receptors) can elicit autonomic hyperreflexia**
*Can also occur after spinal shock resolves and can be a recurrent complication*
32
What are the symptoms associated with autonomic hyperreflexia (dysreflexia)?
* **Paroxysmal hypertension (up to 300mgHg systolic)**
* **Headache-pounding, severe**
* Blurred vision
* **Sweating above the level of the lesion with flushing of** **skin**
* Nasal congestion
* Nausea
* Piloerection caused by pilomotor spasm
* **Bradycardia (30-40bpm)**
* Symptoms may develop singly or in combination
* Can cause serious complications: strokes, seizures, MI, death)
33
How do you treat autonomic hyperreflexia?
* Elevated head of bed
* **Maintain** **free flowing** **urinary drainage** (Drain no more than 600Ml urine at a time) and provide bowel elimination progress
* **Nifedipine (calcium channel blocker) to lower BP and,**
* **Nitrates (nitroglycerin paste or sublingual tablets) to lower BP**
34
How do you treat patients with spinal cord injuries?
* Obtain later and anteroposterior view **x-ray of the spine**
* **MRI of spine** can provide further information regarding cord impingement, hematomas, infraction. **Cord contusion or** **hemorrhage** **cannot be viewed by any other technique.**
* STAT neurosurgery consult
* **Differentiate neurogenic shock (warm, dry extremities, bradycardia) from hypovolemic shock (cool, clammy skin, tachycardia) or other types**
* **For a suspected or confirmed vertebral fracture or dislocation, regardless of** **presence** **or absence of SCI, IMMEDIATE immobilization of** **spine** **is warranted to prevent further injury.**
* Monitor blood pressure very closely. ***Hypotension MUST be avoided to prevent ischemia caused by decreased blood flow and perfusion to*** ***spinal*** ***cord***, which may produce neuronal injury and neurologic deficit. **MAINTAIN MAP at 85-90 mm Hg.**
* **High dose methylprednisolone steroid therapy has been given within eight (8) hours of** **time** **of injury to decrease secondary cord injury**
*
35
What is meningitis?
* **Inflammation of the arachnoid, dura mater, and/or pia mater of the brain and spinal cord (the meninges)**
* Causes of inflammation include *viruses, bacteria or fungal infections*
* The infecting microorganisms gain entry into the nervous system by:
* Spreading through arterial blood vessels
* Direct extension from another site of infection
36
What are some predisposing factors for meningitis?
* Sinusitis,
* Otitis media
* Mastoiditis
* Pneumonia
* Trauma
* Congenital malformations
37
What organisms cause bacterial meningitis?
* **Neisseria meningitides (meningococcus)** \*OCCURS mainly in schools and colleges, and dorms
* **Streptococcus pneumonia (pneumococcus)\***MOST COMMON and most severe; occurs frequently in ***infants or adults with weakened immune systems***
38
What causes bacterial meningitis and how is it spread?
**CAUSE:**
Bacteria inhaled, attach to epithelial cells in nasopharynx where they evade immune defenses cross the mucosal barriers, enter bloodstream, travel to cerebral blood vessels and cross the blood brain barrier and infect the meninges. Bacteria multiply in subarachnoid space and attract large numbers of neutrophils. Release of bacterial endotoxin alter the blood brain barrier, causing cerebral edema and damage brain tissue. The inflammatory exudate thickens the CSF and alters the normal CSF flow around the brain and spinal cord and ultimately causing hydrocephalus. Meningeal cells become edematous and ICP increases.
**SPREAD:**
Disease spread by respiratory droplets and contact with contaminated saliva or respiratory tract secretions (kissing, coughing, sneezing, sharing utensils, food and drink)
39
What is the difference between aseptic/viral meningitis and bacterial meningitis?
CAUSE:
* Pia and arachnoid space are filled with lymphocytes, but not with exudate forms
* **Much more benign and self-limited than bacterial**
* Tends to occur in late summer and early fall
* Transmission usually by cough, saliva, and fecal matter of infected person
40
What types of viruses can cause viral meningitis?
* **Enterovius (MOST COMMON)**
* Arbovirus
* Mumps varicella zoster
* Herpes simplex type 1 and 2
* Epstein Barr virus
* HIV
41
What are the common type of organisms associated with fungal meningitis?
* **MOST COMMON in immunocompromised patients with AIDS through inhalation and bloodstream spread**
* Candida albicans
* Coccidioide immits
* **Cryptococcus** **neoformans** **(MOST COMMON fungal meningitis; found in bird droppings)**
* Histoplasma capsulatum
* Aspergillus
42
What are the clinical manifestations associated with meningitis?
**Infectious signs**
* Fever, tachycardia and chills
**Meningeal inflammatory signs**
* Severe throbbing headache, severe photophobia, nuchal rigidity (stiff neck) and positive Kernig and Brudzinski signs
**Neurologic signs**
* A decrease in consciousness, focal neurological deficits ( cranial nerve palsy, hemiparesis/hemiplegia and ataxia) exaggerated DTRs and seizures,
**Increased ICP**
* Bulging optic disk (indicative of papilledema)
* Vomiting (projectile)
Petechial or purpuric rash involving skin and mucous membranes \*(characteristic of n. Meningitides meningitis)
43
What laboratory/diagnostic tests are done to diagnose meningitis?
* **CT head:** to rule out hemorrhagic stroke
* **Follow-up CT** **post treatment** **in patients with bacterial meningitis, even with improvement, due to** **possibility** **of brain abscess occurring**
* Obtain blood and sputum cultures
* Obtain CBC, electrolytes, coagulation profiles and liver/renal panel.
* **Lumbar puncture** in: Once CT is cleared should be performed
Bacterial findings:
* Appearance of CSF: **cloudy**
* Opening pressure: elevated (greater than 180mm H20)
* Cells: increased WBCs (100-5000/mm – **mostly PMNs))**
* Total proteins: increased (100-500mg/dl)
* Glucose**: decreased (5-40 mg/dl or 0.3 times blood glucose level)**
* Culture: bacteria present on gram stain and culture
Viral Findings:
* Appearance of CSF: **clear, occasionally cloud**
* Opening pressure: usually normal (less than 180mm H2O)
* Cells: increased WBCs (50-1000/mm – **mostly mononuclear cells)**
* Total protein: normal or slightly increased (\< 200mg/dl)
* Glucose: **normal** (greater than 45mg/dl)
* Culture: no bacteria present; demonstration of virus requires special technique)
44
Describe the medical management of a patient with meningitis
* Consult ID
* **Antibiotics must be initiated immediately in those suspected of having meningitis**
Meningococcal meningitis:
* If PCN sensitive: treat with aqueous **PCN G 4 m.u. IV q 4 hours until 5-7 days AFTER** **patient** **becomes afebrile**
* If PCN intermediate sensitive: treat with **Ceftriaxone 2 gms IV q 12 hours or cefotaxime 2 gms IV q 4-6 hours**
Aseptic meningitis:
* Supportive therapy; treat the severely ill with empiric antibiotics
If S. pneumonia is suspected, add:
* **Dexamethasone 0.15 mg/kg IV q 6 hours for 2-4 days**
* Should be administered prior to or with, first antibiotic dose, not after regimen has already started
* Anticonvulsants (lorazepam or diazepam) for acute seizure control
* Acetaminophen 325-1000mg q 4 hours prn pain/fever (DO NO EXCEED 3000mg/24 hours
* IV hydration: Lactated Ringer’s or 0.9NS – avoid hypotonic solutions and D5W
45
What role does a fever have on ICP and CPP in an open head injury?
FEVER causes an increase in increased intracranial pressure (ICP) and cerebral perfusion pressure (CPP)
