SSEP or Somatosensory Evoked Potential is a measurement of the electrical potentials produced in response to a stimulation of the sensory system. The electrical stimulation is made through a skin or needle electrode using sqaure wave stimulus (duration 0.2 - 2 ms, rate 1-2 Hz). The common stimulation site includes median n., ulnar n., post. tibial n., common peroneal n. , etc.

There are 2 forms of EPs - short and long-latency. The short-latency SSEPs is the one that is used intraoperatively because they are less interfered by anesthetic depth and other intraoperative factors.

Short-latency SSEPs potentials produced by stimulation of the median nerve at the wrist ( from ref no.1)

Sensory nerves (with the cell bodies in the dorsal root ganglia) processes signal rostrally (first order fibers), ipsilaterally in the post. column to synapse in the dorsal column nuclei at cervicomedullary function then signal thru the second order fibers -crossing to contralateral thalamus via the medial lemniscus which send the third order fibers from thalamus to frontoparietal sensorimotor cortex

The effects of anesthetic drugs/inhalational agents on SSEPs, BAEPs (Brainstem Audiotory Evoked potentials), VEPs (Visual EPs) and Transcranial MEPs can be summarised as the following table. Please note that the VEPs are the most sensitive and BAEPs are the most resistant to drug effects.

SSEPs BAEPs VEPs Transcranial MEPs Drugs LAT AMP LAT AMP LAT AMP LAT AMP Isoflurane 0 P Enflurane 0     Halothane 0 0 N2O 0 0 0 a Barbiturates 0 Pb Pb Etomidate     0 Propofol     P Pb Droperidol            c Diazepam 0 0         Midazolam 0          P P Ketamine 0           0 Fentanyl 0 0     0 0 Morphine             Meperidine /             LAT - latency, Amp-amplitude, P-prohibitive in clinically useful dose a P if inspired concentration > 50% b Following bolus administration; low dose infusions may be acceptable in some cases c Drug not given during general anesthesia; volunteers awake following administration dose

-All the volatile inhalation depress the SSEPs, the desflurane and sevoflurane have qualitatively and quantitatively similar effects as isoflurane. The degree of these depressant effects on SSEPs between Halothane and Isoflurane or enflurane is somewhat controversial. Generally, 0.5-1 Mac of both halothane and enflurane in N2O has been reported in use with preservation of SSEPs.

-Opioid also cause dose-dependent decreaes in amplitude and increases in latency except for meperidine which can increase the amplitude. The uses of opioid during intraoperative SSEPs is acceptable, even with high doses. However, the large IV bolus should be avoided at the times of potential surgical compromise to neurologic function.

-Besides of pharmacologic effects on SSEPs, other physiologic effects e.g. systemic BP, temperature, blood gas tensions, anemia, etc can also influence SEP recordings. Again, BAEPs seem to be the most resistant to these physiologic alterations.

Hypocarbia or hypocapnia is most commonly seen in hyperventilation in mechanically ventilated patient. In other clinical settings, hypocarbia can be found in hyperventilation syndrome, respiratory compensation in chronic metabolic acidosis, asthma (early), etc

Cardivascular effects
   - decrease the inotropic state of the heart (withdrawal of sympathetic nervous system activity, decreased ionized Ca)

Respiratory effects
   -respiratory alkolosis leads to hypokalemia, hypocalcaemia
   -decrease QT by : increased intrathoracic pressure (which decrease the CO)
   -inhibit HPV (causing bronchoconstriction and decrease CL)
   -passive hypocapnia can produce apnea (reduced respiratory drive)

CNS
    -decrease cerebral blood flow by induced cerebral vasoconstriction, risk of seizure is increased if enflurane is used.

Others
    -shifts oxy-Hb curve to the Lt, decrease O2 unloading.
   -induced vasoconstriction -> decrease peripheral flow
   -reduced placental blood flow

Early prevention of hypothermia is the most successful method. Pre-warming the patient prior to induction (via forced-air blanket) decreases heat loss during the first hour after induction. However, in case of hypothermia, methods for rewarming includes :

1.) Forced-air blanket over the body parts not involved in surgery.
2.) Comfortable room air temperature ( about 20 c)
3.) Keep the patient covered all the time.
4.) Heat and moisture exchanger. (read the editor comments here)
5.) Low flow and closed circuit anethesia technique.
6.) Radient heat lamps (more effective for neonates and infants)
7.) pre-warmed IV fluids.
8.) Fluid warmers for blood and blood products transfusion.

The most effective method for rewarming cold postop. patient is the use of forced-air warming blanket device.

Anesthetic agents can cause the reversible effects on many cerebral physiologic factors including cerebral blood flow (CBF), cerebral metabolic rate (CMR) and electrophysiologic function (e.g. EEG, EPs). These changes can adversely affect the diseased brain but maipulation of anesthestic technique to achieve the changes in the correct way can be beneficial to the patients, too.

Normal adult human brain weigh approximately 1400 gm or 2 % of body weight and receive about 12-15 % of CO due to high cerebral metabolic rate. The O2 consumption is about 3.5 ml per 100 gm of brain tissue or 49 (14 x 3.5) ml/min which represents about 20% of total body O2 consumption. Cerebral autoregulation or myogenic regulation plays an important role in maintaining cerebral perfusion. Cerebral perfusion pressure (CPP) is the MAP - ICP and normally is maintained by autoregulation between MAP of 50-150 mmHg. The normal cerebral physiologic values is shown in the table below.

There are many physiologic factors or non-anesthetic drugs that can influence CBF e.g. temperature, CO2, O2, vasoactive agents, blood viscosity, etc. In this chapter, we will discuss only the impacts on cerebral blood flow from anesthetic agents.


Intravenous Anesthetic Agents

   Most IV anesthetic agents (except for Ketamine) cause a reduction in CMR and CBF. The paralell or coupled efffects of a reduced CMR and then decreased CBF is one of the explanations. There is also a direct effect of IV anesthetic agent on cerebral vascular smooth muscle that contribute to the net effect as very well known that barbiturates is a cerebral vasoconstrictors.

Changes in cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) caused by intravenous anesthetic agents. The data are derived from human investigations and are presented as a percentage of change from unanesthetized control values. No data for the CMRO2 effects of midazolam in humans are available.

Inhaled Anesthetics
All the volatile anesthetics cause a dose-related reduction in CMR while simultaneously causing no change or an in crease in CBF (called "uncoupling" effect of flow and metabolism). These effects are seen more in Halothane >> enflurane > isoflurane = sevoflurane = desflurane. In clinical, the uses of 1 Mac isoflurane doesn't seem to cause much trouble with increase ICP, but it's been clearly demonstrated that hypocapnia prior to introduction of inhaled anesthetic (Halothane) , the increased ICP can be prevented or greatly attenuated. Overall, the isoflurane or desflurane or sevoflurane are more preferrable than halothane.
   N2O has been studied extensively and the available data indicate unequivocally that N2O can cause increase in CBF, CMF and ICP. The severity varies considerably to the presence of absence of other anesthetic agents. Usually, addition of N2O to an established volatile anesthetics results in moderate CBF increases. When administered with IV anesthetics (except for Ketamine), the CBF effect may be considerably reduced.

Estimated changes in cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) caused by volatile agents. The CBF data for halothane, enflurane, and isoflurane were obtained during 1.1 MAC anesthesia (with blood pressure support) in human patients,270 expressed as a percentage of change from awake control values. The CMRO2 data for halothane, enflurane, and isoflurane were obtained in the cat and are expressed as a percentage of change from nitrous oxide (N2O)–sedated control values. The data for sevoflurane were obtained during 1.1 MAC anesthesia in the rabbit and are expressed as a percentage of change from a morphine/N2O–anesthetized control state.

Muscle relaxants
Nondepolarizing muscle relaxants
   Otherwise than the histamine release effect from some non-depo MR e.g. d-Tubocurarine, metocurine, mivacurium, atracurium, etc ,the non-depo MR per se, has no significant effects on the CBF. Histamine can cause a reduction in CPP because of simultaneous increase in ICP (from cerebral vasodilation) and decrease in MAP. The indirect effect of non-depo MR includes
     -the vagolytic effect from pancuronium may induce hypertension and elevated ICP.
     -the use of MR attenuates or prevents the coughing/straining which may help in reducing ICP.

Succinylcholine
   Succinylcholine cause an increase of ICP which is not correlated with the degree of fasiculation. The role of precurarizing dose and increased ICP is still controversial, in Vecuronium and metocurine defasciculation dose has been demonstrated in human but no studies with the other nondepoMR.
   However, the uses of succinylcholine is not contraindicated in the situation that rapid intubation is indicated, given that the induction dose of IV anesthetics is adequate, no arousal phenomenon and perhaps the uses of defasciculating dose (metocurine/vecuronium) has been given prior.

Introduction

The annual incidence of traumatic spinal cord injury (SCI) ranges from 11.5-53.4 per million. Currently there are > 250,000 SCI people living in the United States. Aproximately 10,000 new injuries each year.

Majority of SCI are related to MVA, male between 15-25 years . The most frequent level of cervical SCI is C5-6, thoracic SCI is T12-L1. The mortality rate is 48%, mostly in the younger and older patients. SCI are found associated with other trauma in 25-65% of cases e.g. head injury, other soft tissue injuries, most suspicious in the patient who display brain stem or cerebellar dysfunction.

Spinal cord blood flow (SCBF) is autoregulated in the same fashion as cerebral blood flow, between the range of 50-150 mmHg. The CO2, O2 directly influences the SCBF.

Pathophysiology

Following the SCI, initially, the injury involves the gray matter (the central part), the small blood vessels in the gray matter disrupted, endothelial breakdown and causes subsequent hemorrhage and edema and further causes a rapid decrease in SCBF. Hypoperfusion in the white matter follows, loss of local autoregulation, decreased tissue O2 tension, increased lactic acid Spinal cord ischemia, potentially spread caudally and rostrally. The biochemical cascade leads to the release of potent vasoconstrictor -> further ischemia, generation of free radicals, lipid peroxidation. Necrosis of neuronal tissue, within 24 hrs, the central gray and adjacent white matter becomes necrotic.

   SCI also causes the systemic disturbances mainly involved in autonomic nervous system. The consequences of SCI include

   1.) Autonomic hypo-/hyperactivity : mostly SCI above T5. Initially, there is an immediate hypertension and then within minutes, becomes hypotension due to the interruption of spinal sympathetic tracts which causes the pooling of blood in the dilated peripheral vascular beds (like spinal block). Bradycardia is due to the unopposed parasympathetic and the severed cardioaccelerator fibers from T1-4. This may jeopardize patients for the unability to maintain the adequate CO.

   2.) Spinal shock : mostly in the spinal cord transection. There is a complete loss of somatic/visceral sensation, flaccid paralysis, absent deep tendon /abdominal reflexes and plantar responses, retention of urine and feces. Severe hypotension. Spinal shock may last 3 days - 6 weeks. The resolution of spinal shock is indicated by the return of elicited spinal cord reflex arc.

   3.) Pulmonary edema : the most common cause of death from acute SCI, prevalence is > 40%. This is caused by overzealous fluid replacement or neurogenic response (involves transient, centrally mediated sympathetic discharge, predominatly a-adrenergic, leads to a shift of blood from high-resistance peripheral vascular beds to the low-resistance pulmonary bed)

Treatment
   -Early treatment (within 8 hours) may spare the adjacent white matter and minimize the degree of functional impairment. The effective treatment is methylprednisolone (large doses), the other proposed therapeutic modalities but not proven includes naloxone, TRH, local hypothermia, HBO, catecholamine antagonists, dimethyl sulfoxide, gangliosides, diuretics, Ca channel blocker.
   -The vertebral column should be stabilized at the scene. The SCI must be assumed in all comatose injured patients until proven otherwise. The lesion above C4 will require assisted ventilation. The clinical criteria that may suggest for intubation include
        * PaO2 < 100 mmHg, PaCO2 > 45 mmHg
        * Maximum inspiratory force < 20 cmH2O
        * Vital capacity < 15 ml/kg
        * PaO2/FiO2 ration < 250
        * Abnormal CXR reveaing atelectasis, pulmonary edema or pulmonary infiltration.
   -Hemodynamic instability is encountered, appropriate intravascular volume repletion is required which may mandate the use of PA catheter. The judicious use of IVF is very important and must be counterbalanced between providing adequate SCBF and minimize the risk of pulmonary edema. Atropine or Isoproterenal may be used in severe bradycardia.
   -Pulmonary complications are the most common cause of death. Patient who has SCI above C5 will lose the diaphragmatic innervation, demands ventilatory support. For lower injury, the paralysis of intercostal and abdominal muscles lead to an ineffective cough, decreased vital capacity, VT, TLC, ERV, FEV1, FVC, EFR and FRC. The chest physiotherapy, percussion, breathing exercises has been shown to decrease the pulmonary complications. Tracheal suctioning has been associated with bradycardia and cardiac arrest (due to unopposed vasovagal reflex).
   -Gastric atony or paralytic ileus is common during the first 2 weeks which causes further respiratory deterioration.
   -Surgical treatment is indicated in SCI to achieve alignment when non-surgical treatment has failed, or to decompress an injured spinal cord, to stabilize persistent subluxation and to treat any accompanying injuries.

Anesthetic management
1.) Preoperative evaluation
   -careful assessment of respiratory and hemodyamic status which may include ABG, bedside PFT, PA cattheter, EKG
   -beware of other occult associated injuries, the hemorrhagic shock can present despite the pulse rate < 60.
   -Routine electrolytes must be checked and corrected.
   -Premedication if needed, must be given with extra cautions. Atropine is very useful in those whose pulse rate < 70.

2) Intraoperative Management
   -Routine monitorings and extra monitorings e.g. PA catheter, CO, SSEP, ICP monitor, A-line
   -Considered full stomach due to gastric atony, paralyzed abdominal mucles, supine position, stress induced delayed gastric emptying time. Cricoid pressue must be done carefully in the patient who has cervical SCI.
   -Method of intubations depends on patient's status. An awake intubation, fiberoptic intubation, manual in-line stabilization, Fast-Trach, retrograde intubation, tracheostomy, etc has been performed successfully. The goal is to maintain the neck stability and minimize further cord injury.
   -Succinylcholine is relatively contraindicated in acute SCI and absolutely contraindicated in subacute or chronic SCI
   -Careful positioning, especially in the cervical SCI. The awake positioning after intubation followed by induction has been reported. Rapid sitting up can lead to hypotension and even cardiac arrest. If the patient remain in head-down position, pulmonary edema and LV failure can occur.
   -Hemodynamic instability may be further depressed by anesthetic agents, slow careful induction and dosing is recommended. Anesthetic technique should allow timely neurologic examination at between or the end of surgery.
   -SCI at above T1 will impair the thermoregulation.

3) Postoperative care
   -Extubation and weaning off the ventilatory support must be done with caution even with the patient who spontaneous breath adequately, preoperatively. Incentive spirometry and chest physiotherpy should be continued. Patients will need to be monitored in the ICU or SCI unit further.

Cervical instaility is most commonly found in Down syndrome or in the un-immobilized cervical spine injury patient. In Down syndrome, the cervical instablity is due to the ligamentous laxity which is caused by underlying collagen defect which then result in atlantoaxial (10-20%) and atlantooccipital instability(61-63%). The cervical instability in Down syndrome may be also associated with anomalies of the upper cervical spine.

Neurological Findings
The symptoms are present only 1-2.6 %. Usually the instability is discovered on routine screening examinations or cervical roentgenogram. The progressive instability that lead to neurological symptoms is most common found in boys > 10.5 years of age. Involvement of pyramidal tract results in gait abnormalities, hyperreflexia and motor weakness. Other symptoms may include neck pain, occipital headaches and torticollis. The SSEP has also been used to detect a neurological involvement in the un-cooperative Down syndrome patients.

Roentgenographic Findings
The X-ray should be done in antero-posterior, flexion, extension and odontoid views. An atlantodens interval (ADI) of > 4-5 mm is indicative of instability. If the ADI > 6-7 mm, MRI or CT scanning in flexion and extension is neccessary to evaluate the available space for spinal cord.

Pseudotumor cerebri or benign intracranial hypertension or idiopathic intracranial hypertension is described in the clinical settings characterized by
   1. Increased ICP (>20 and as high as 60 cmH2O) that is not related to a pathologic process
   2. normal CSF composition, and
   3. no alteration in consciousness

Pseudotumor cerebri presents in 2 clinical age groups - infantile and adult

Infantile form : patients present with rapid head growth, split sutures, tense fontanelles with normal developmental milestones. CT shows enlarged ventricles and fluid spaces over the brain.

Adult form : predominantly found in female, commonly in obese women who complains of headache, nausea, vomiting and dizziness or blurred vision without other signs of cerebral dysfunction. The headache is typically worsed in the AM and aggravated by head movement or vasalva. The visual complaints usually begins from diplopia, bluured vision or blindness. The visual field examination reveals enlarged blind spot and inferonasal field deficit.

   The symptoms is usally self-limted but 10 % of patients may have residual visual impairment (from prolonged papilledema). The symptoms can vary with weight, menstrual cycle, pregnancy, OC uses.

   Physical examination is usually unremarkable other than the papilledema. CT may show normal or small lateral ventricles with slit third ventricles and effaced cerebral sulci.

   The cause(s) of pseudotumor cerebri can be summarized as the table. Usually, the single cause cannot be identified and there are many proposed mechanisms to explain the pathophysiology.

Treatment
   -Patients should be encouraged to lose weight, generally the symptoms responds to medical treatments e.g. furosemide, acetazolamide and dexamethasone.
   -Serial lumbar punctures (to remove about 30 ml of CSF or until 50% reduction of the opening pressue achieved) have been recommended to alleviate symptoms.
   -Surgical treatment is considered in whom the medical treaments fail or the visual symptoms progress. The CSF diversion procedure e.g. lumboperitoneal shunts or other sunts exhibit failure or require reoperation in < 6 months. For visual dysfunction, the procedure like optic nerve sheath decompresion can reverse or stabilize the visual loss and may lead to resolution of headache.

Anesthetic concerns.
   -These patients are different from hydrocephalus. The spinal or epidural anesthesia are not contraindicated. Lumbar puncture is safe and beneficial and there is no reports of variations in the dermatomal spread of anesthesia from normal population. In the patients who have the LP shunt device, spinal or epidural may be contraindicated due to the possibilities of damaging the device or loss of local anesthetic agents through the device.

It defines the severity of neurologic impairment following head trauma in terms of eye opening, speech and motor fucntion. The scale score ranges from 3-15. Severe head injury is defined as score of < 7 or lesss, persisting for 6 hour or more.

In the infants, the GCS has been modifed as

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Subarachnoid hemorrhage (SAH) occurs when there is a bleeding into the subarachnoid space. The most common cause is rupture of the intracranial aneurysm which presents in over 5 million people in the North Americans and approximately 28,000 cases of SAH occur annually. The peak age is 40-50 years of age. The SAH in the patient < 20 yo, mostly is from the AVM rupture. There is a linear relationship between aneurysm size and risk of rupture except for the giant aneurysms (>2.5 cm) because of thrombosis and calcification.

The presence of blood in the subarachnoid space causes an abrupt, marked increase in ICP, which then often result in systemic hypertension and bradyarrhythmia (Cushing's effect). The clinical presentations are severe abrupt headache associated with N/V, stiff neck, photophobia, and often transient loss of consciousness.
   In about 50% of patient may present with small bleed or "warning leak"precedes a major aneurysmal rupture. Those symptoms and signs tends to be mild and non-specific e.g. headache, dizziness, orbital pain, slight motor or sensory disturbance.

Initially, following the SAH, the rebleeding is the most common complications which affect the morbidity and mortility outcome (50% death, the survived 50% has often poor outcome). The risk of rebleeding is 4% in the first 24 hr. Then after 48 hr, it's 1.5 % per day with a cumulative risk of 19% for over the initial 2 weeks.

After recovering from SAH, another major complication is a vasospasm which is found symptomatic in approximately 30% of the patients, most often between days 4 and 12, with a peak at 6-7 days. The clinical symptoms include worsening headache and increasing blood pressure, may followed by progressive lethergy, focal motor and speech impairments (corresponding to the brain area that's involved). The vasospasm may resolve gradually or progress to coma and death within a period of hours to days.

There are several grading system used to determine the prognosis of SAH e.g. Hunt and Hess, World Federation of Neurosurgeon (WFNS grade) SAH scale. Usually, the higher grade, the worse of the prognosis and outcome.