Книги по МРТ КТ на английском языке / Neurosurgery Fundamentals Agarval 1 ed 2019

18.2  Neuroanesthesia

18.2.1  Modifiable Parameters

Parameters relevant to Neurosurgery that can be modulated by the Anesthesiologist include blood pressure which helps to determine a patient’s cerebral perfusion pressure (CPP), jugular venous pressure, arterial carbon dioxide tension, arterial oxygen tension, hematocrit, temperature, blood glucose level, CSF output, level of the patient’s head, intravascular volume, and body position. Many of the above-men- tioned parameters can affect the intracranial pressure (ICP), CPP, and mean arterial pressure (MAP). All of which together affect your patients’ cerebral blood flow (CBF) as well as their cerebral metabolic rate of oxygen consumption (CMRO2).24,​25

18.2.2  Drugs Inhalational Agents

These agents, except for nitrous oxide (N2O), suppress neuronal activity and thus reduce cerebral metabolism. These agents do cause some degree of vasodilation which can increase cerebral blood volume and thus increase ICP.

N2O is a potent vasodilator and can markedly increase CBF, with minimal increases in cerebral metabolism.

N2O may convert a pneumocephalus to a tension pneumocephalus as it is much more soluble than nitrogen, so it is more likely to precipitate out of solution.

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N2O can also cause an acute B12 deficiency by directly deactivating the B12 molecule.

Halogenated agents include isoflurane (Forane), desflurane (Suprane), and sevoflurane (Ultane). All of these agents suppress EEG activity and have been theorized to provide some degree of cerebral protection.24

Intravenous Agents

These agents are often used for induction of anesthesia as well as often being used for conscious sedation and include propofol, barbiturates, etomidate, and ketamine.

Propofol has a short half-life allowing for repeated neurologic examinations in those under sedation. There is a dose-­ dependent drop in MAP and thus ICP.

The adverse effects are often monitored by following triglyceride levels and watching for metabolic acidosis.

Large continuous dosing can cause propofol infusion syndrome consisting of metabolic acidosis, cardiac failure, rhabdomyolysis, renal failure, and other abnormalities including eventual death.

Barbiturates can produce significant decreases in cerebral metabolism and suppress EEG activity all the way to burst suppression or electrographic silence. Most are used orally as antiepileptic drugs or used intravenously to treat status epilepticus. All forms may cause dose-dependent hypotension. The most commonly used IV agent is sodium thiopental (Pentothal) as it has a rapid onset and shortest half-life.

Etomidate (Amidate) is an anesthetic with amnestic but no analgesic properties. It can produce myoclonic activity. It has also been known to impair renal function and may produce adrenal insufficiency. It is a very hemodynamically stable agent to use for induction, often the drug of choice

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for induction with patients who have increased ICP.

Ketamine produces a dissociated anesthesia with very little effects on cardiac output or respiratory function. In the past, its use was avoided in those with increased ICP, as it was thought to cause some mild increase in heart rate and blood pressure leading to increased ICP. However, this is not proven and in those with hypotension you may argue for its use. Patients should be monitored for paradoxical agitated delirium with prominent hallucinations and agitation.24,​25

Narcotics

These agents can all slow the EEG but will not produce electrographic silence. They all cause dose-dependent respiratory depression and thus can cause hypercarbia leading to cerebral vasodilation and increased ICP in nonventilated patients.

Nonsynthetic agents, including morphine, may produce hypotension, vaso­ dilation, and its excretion is impaired in those with renal insufficiency. Meperidine (Demerol), which has neuroexcitatory metabolites, can cause hyperactivity as well as seizures.

Synthetic narcotics, including fentanyl, sufentanil (which can cause increases in ICP), alfentanil (which can also raise ICP), and remifentanil, can be used in awake craniotomies. These agents, unlike the nonsynthetic agents, do not lead to histamine release. This means that they cause less hypotension and thus less effects on patient’s CPP.

Miscellaneous Drugs

Benzodiazepines produce anticonvulsant action and produce amnesia. Those commonly used for anesthesia or sedation include lorazepam or, the now more popular, midazolam.

Lidocaine suppresses the laryngeal reflexes and can help blunt ICP elevations especially during intubation. It is used by some as pretreatment for those being intubated who have known elevated ICP. ­Fentanyl is more commonly used in this situation.

Esmolol can also be used to blunt the sympathetic response to intubation, although in emergent situations where blood pressure may be in flux, the use of a

β-blocking agent may be problematic, lim- iting its use.

Dexmedetomidine (Precedex) is cen- tral α2-adrenergic agonist which has multiple uses including sedation, control of postoperative hypertension, agitated delirium, withdrawal symptoms, and sedation during awake craniotomy.24,​25

Paralytics for Intubation

To facilitate endotracheal intubation, paralytics are used in conjunction with induction agents. Succinylcholine is the drug of choice of rapid sequence intubation in those acutely neurologically ill patients with elevated ICP due to its rapid onset and short duration of action.

There are cases where other agents such as rocuronium should be used. These include those with or at risk for hyperkalemia, those with disuse atrophy, or those with neuromuscular junction disorders, such as myasthenia gravis, in which the depolarization neuromuscular blocking effect of succinylcholine can be prolonged.24,​25

18.2.3  Evoked Potentials

Stimulation of sensing organs or peripheral nerves leads to responses in their

corresponding cortical areas and in the interconnecting subcortical areas. These pathways cannot all be directly measured. However, their representative areas can be detected with specific electrode placement and by using computers to average inputs forming waveforms. The latencies and amplitudes can be measured and followed to help with diagnostic reasons as well as for monitoring during neurosurgical interventions.

Anesthetics can have effects on the evoked potentials, which are being monitored during neurosurgery. All volatile agents produce dose-dependent reduction in somatosensory-evoked potentials (SSEP).

Generally using the minimal effective dose is required, staying away from barbiturates and volatile agents. Using continuous infusions versus intermittent boluses will minimize anesthetic effects on evoked potential monitoring.24

18.2.4  Malignant Hyperthermia

Presentation

This is a hypermetabolic state in which one observes rapidly rising body temperature, and extreme muscle rigidity. It is often associated with the use of volatile inhalation anesthetics (e.g., halothane) or succinylcholine.24

Treatment

Discontinuation of the offending anesthetic agent and treatment with dantrolene sodium (Dantrium) at a dose of 2.5 mg/kg IV, infuse until symptoms improve up to 10 mg/kg.

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Prevention

Patients at risk include those with a ­family history of malignant hyperthermia, heavy musculature, muscular dystrophies (particularly Duchenne’s type), or scoliosis. For those at risk, avoid use of succinylcholine and use nonhalogenated anesthetics.24

18.3  NeuroOphthalmology

18.3.1  Nystagmus

Nystagmus refers to either a spontaneous or induced oscillation of the eyes that begins with a slow phase and may or may not have a quick corrective saccadic correction. The direction of the nystagmus is named for the direction of the quick phase. Horizontal or upbeating gaze-provoked nystagmus has a large differential diagnosis, including medications like antiepileptic drugs (AEDs). Vertical nystagmus which is not gaze-evoked, especially if down ward beating, is very concerning for brainstem pathology.26,​27

18.3.2  Papilledema

Papilledema refers to optic nerve swelling secondary to increased intracerebral pressure believed to cause axoplasmic stasis,­

and most of the time is bilateral. Causes include direct compression from tumors, vascular disease such as anterior ischemic optic neuropathy or vasculitis, Foster ­Kennedy syndrome, and demyelinating disorders. Over time, it will lead to optic nerve damage and can cause permanent loss of visual acuity.28

formal testing, can help with diagnostics, following disease progression, and determining driving safety. Normal visual fields are about 50 degrees above and below the horizontal meridian, 35 degrees nasally, and 90 degrees temporally. About 15 degrees nasally from the fovea lies the optic disc, at that point on the retina there are no photoreceptors. This creates the physiologic blind spot lying about 15 degrees temporally and slightly inferior from the point of central fixation.29

Visual Field Deficits

These can be tested for by bedside confrontation testing which should be performed on each eye individually. Formal testing can be performed using tangent screens, Goldmann’s perimetry or Humphrey’s visual field (automated perimetry) examinations.

Visual field deficits are often described regarding location and extent of the lesion. For lesions affecting just one eye, they are often referred to as scotomas. Complete visual loss is referred to as anopia. The rest of the lesions are referred to by their location (right, left, inferior, superior) and size (hemi-, quadrant-). Fig. 18.6 shows common lesions and their associated areas of damage.29

18.3.4  Pupillary Diameter Pupillodilator and Tract

The pupillodilator muscle is a set of muscle fibers which act on the iris and when contracted, the pupil dilates.27

18.3.3  Visual Fields Introduction

Visual field testing is an important bedside testing maneuver and, with more

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Pupilloconstrictor and Tract

The pupilloconstrictor muscle consists of muscle fibers that narrow the pupil when they contract.27

Afferent Pupillary

Defect (Marcus Gunn Pupil)

This phenomenon is seen when the direct and consensual pupil response to light when stimulating the affected eye are decreased or absent, while the direct and consensual pupil response when stimulating the unaffected eye to light is normal.30

Light-Near Dissociation and Argyll Robertson Pupil

With light-near dissociation, the pupils do not constrict as strongly to light as compared to constriction seen with testing of accommodation. When referring to this finding in relation to neurosyphilis, it is known as the Argyll Robertson pupil.

However, it is associated with other etiologies such as dorsal midbrain syndrome, vascular disease (such as diabetes or alcohol leading to cranial nerve [CN] III dysfunction), and in those with Adie’s pupil.30

Anisocoria

Anisocoria refers to unequal pupil sizes usually more than 1 mm.30 A physiological anisocoria less than 1mm in difference can be seen in roughly 20% of the population.

Adie’s Pupil

Adie’s myotonic pupil, or a tonic pupil, is due to a lesion of postganglionic parasympathetic fibers and the true etiology is often unknown. If the patient has

associated decreased reflexes, it is then referred to as Holmes–Adie syndrome, which is more commonly seen in young women.

Slit-lamp examination will reveal that some parts of the iris are contracting while others are not. If the pupillary abnormality has been present for several weeks, there has been enough time for hypersensitivity of the acetylcholine receptors on the iris to develop and if dilute pilocarpine is applied (0.125%), about two drops, the dilated eye will exhibit miosis.30

Pharmacologic Pupil Although mydriatic agents are used commonly to perform a dilated eye examination, there are times when patients may be exposed to mydriatic agents and are unware of this, leading to their presentation to a clinician for pupillary abnormalities. This should normalize with time.30

Cranial Nerve III Compression

Cranial nerve III compression can initially manifest with pupillary dilation as the parasympathetic fibers travel in the periphery of the nerve where they are vulnerable to mechanical compression. Etiologies include aneurysm expansion, tumor compression, and uncal herniation.30

Horner’s Syndrome

Horner’s syndrome is a triad of miosis, ptosis, and anhydrosis. This set of symptoms occurs when there is disruption of the sympathetic innervation to the face and eye. Miosis occurs due to denervation of the pupillodilator muscle. Ptosis occurs due to denervation of Müller’s muscle. This only leads to a minor ptosis which is not complete. Anhydrosis is secondary to denervation of the sweat glands. Differential diagnosis includes lateral medulla infarction, Pancoast’s tumor, and carotid dissection.27

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18.3.5  Extraocular Muscles Introduction

The extraocular muscles are made up of six striated muscles that are under the control of three cranial nerves which direct eye movement. The cranial nerves that have direct control over the extraocular muscles are CN III (oculomotor), CN IV (trochlear), and CN VI (abducens).31

Intranuclear Ophthalmoplegia

Lesions to the medial longitudinal fasciculus (MLF) will produce a syndrome known as intranuclear ophthalmoplegia. This syndrome consists of poor adduction ipsilateral to the lesion as the MLF conveys information between the contralateral abducens nucleus and the ipsilateral oculomotor nucleus. At times, patients may have nystagmoid beating of the abducting eye. Common causes include MS, other demyelinating lesions, and cerebrovascular accidents.32

CN III (Oculomotor) Palsy

Complete Oculomotor Palsy

The classic complete CN III palsy is that of the “down and out” eye, which consists of ocular depression and abduction. There is associated mydriasis due to loss of parasympathetic innervation and severe ptosis due to loss of the levator palpebrae superioris.33

Non-Pupil-Sparing Oculomotor Palsy

When the pupil is not spared, the pathology usually involves extrinsic compression of the third cranial nerve as the parasympathetic fibers travel along the periphery of the nerve.

Common etiologies include tumors, vascular lesions such as aneurysm, uncal herniation, and cavernous sinus lesions.

Pupil-Sparing Oculomotor Palsy

In these patients, there will be weakness of the motor component of the third cranial nerve, however, the pupillary function will remain intact. This is believed to occur usually due to vascular compromise of the small vessels feeding the nerve itself. Common etiologies include diabetic mononeuropathy, atherosclerosis, and vasculitis.

CN IV (Trochlear) Palsy

The trochlear nerve is unique in that it is the only cranial nerve to exit from the dorsal aspect of the brainstem and that it is the only completely crossed cranial nerve. Patients with a trochlear nerve palsy may present with diplopia and often have some compensation which is achieved by tilting their head opposite of the affected eye. Common etiologies of CN IV palsy are trauma, congenital palsies (with decompensation later in life), and small-vessel disease. However, most of the time the etiology is idiopathic.33

CN VI (Abducens) Palsy

Patients with lesions affecting CN VI will experience horizontal diplopia at distance due to loss of function of a lateral rectus muscle. Common etiologies for an abducens palsy include changes in ICP, diabetic mononeuropathy, vasculitis, and cavernous sinus lesions.33

Orbital Pseudotumor

Orbital pseudotumor is an inflammatory orbital disease in which patients have idiopathic inflammation of the extraocular muscles, their tendinous insertions, and

the other orbital contents. This is not due to changes in ICP. In most cases, this is a unilateral phenomenon and responds to steroids.34,​35

Tolosa–Hunt Syndrome

Tolosa–Hunt syndrome presents as unilateral orbit pain with accompanied oculomotor paresis. These findings are like those found with structural or anatomic lesions, and MRI may reveal a focal enhancing mass. Tolosa–Hunt is secondary to granulomatous inflammation of the cavernous sinus and may extend to the superior orbital fissure and orbit itself. Of note, this may be the presenting sign/ symptom of neurosarcoidosis. This syndrome responds well to corticosteroid treatment.35

Raeder’s Syndrome

Raeder’s syndrome is also known more precisely as paratrigeminal oculosympathetic syndrome consisting of unilateral pain in the distribution of the trigeminal nerves ophthalmic division along with at least a partial Horner’s syndrome with unilateral ptosis and miosis. This constellation of syndrome can be associated with a carotid artery dissection.36

Gradenigo’s Syndrome

Gradenigo’s syndrome consists of a triad of periorbital unilateral pain, diplopia, and persistent otorrhea. The periorbital facial pain comes from involvement of CN V and diplopia due to CN VI dysfunction. This used to be associated with bacterial otitis media with apex petrositis (inflammation of the petrous portion of the temporal bone). In the post-antibiotic era, the triad seen in Gradenigo’s syndrome secondary to otitis media has become rare and the triad is now more often associated with

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cholesteatomas, other tumors/cancers, or even chronic osteomyelitis of the petrous bone.37

18.3.6  Miscellaneous Signs Corneomandibular Reflex

The corneomandibular reflex, sometimes referred to as the Wartenberg reflex, consists of contralateral deviation of the jaw following tactile stimulation of the cornea. It is believed to be due to severe supranuclear eye movement center dysfunction of the rostral brainstem. It is a rare sign, however, when present indicates upper brainstem area dysfunction and can help with localization in the comatose patient.38

Duane’s Syndrome

Duane’s syndrome is a congenital disorder in which patients can have a variety of extraocular motor abnormalities. Duane’s syndrome has three different types: type 1 consists of an inability to abduct the affected eye; type 2 consists of an inability to adduct the affected eye; and type 3 consists of an inability to both abduct and adduct the affected eye. These patients will have normal alignment upon primary gaze and due to suppression, despite obvious extraocular motion abnormalities, will not complain of double vision. Patients with type 1 Duane’s syndrome will classically have narrowing of the palpebral fissure as well as globe retraction that occurs when the eye is moved into adduction.39

Hippus

Hippus is a normal phenomenon that is most commonly seen when testing the pupillary light reflex in patients. Hippus describes small spontaneous oscillation of the pupil. Simply wait until the

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hippus abates prior to measuring pupillary size.40

Ocular Bobbing

Ocular bobbing is a physical examination sign that consists of rapid conjugate downward eye deviation followed by a slow return of the eyes to the primary position. This finding is usually accompanied by bilateral horizontal gaze palsy and indicates a destructive pontine lesion usually involving the bilateral paramedian pontine reticular formations, which are the supranuclear control centers of horizontal gaze. This is different from ocular dipping consisting of a slow downward deviation and fast return to primary position, which is a rather nonspecific finding lacking localization value.41

Opsoclonus

Opsoclonus (saccadomania) consists of back to back conjugate saccades without an intersaccadic interval and is multi­ directional with horizontal, vertical, and torsional components. This is always abnormal and common causes include viral encephalitis, paraneoplastic syndromes, drug intoxication (such as lithium), and classically in the opsoclonus–myoclonus syndrome seen in children with a neuroblastoma.41

Oscillopsia

Oscillopsia is the term used to describe the illusion of environmental motion or blurred vision. This is usually seen in patients with abnormal spontaneous eye movements like an acquired nystagmus. Patients with congenital forms of nystagmus often do not report oscillopsia, even if their spontaneous eye movements are readily visible on examination.41

18.4  Neurotology

18.4.1  Vertigo Differential Diagnosis

When medical practitioners are seeing a patient complaining of dizziness, the initial differential is quite daunting, ranging from vascular, inflammatory, infectious, neoplastic, degenerative, drug mediated, congenital, autoimmune, traumatic, endocrine, or metabolic disturbances. Examination techniques, such as the Dix–Hallpike maneuver ( Fig. 18.7), are useful in examining the vertiginous patient. If nystagmus is present, examination and documentation of the nystagmoid eye movement in a variety of directions of gaze can help direct further management and work-up.42

Vestibular Neurectomy

Surgical Considerations

Two conditions in general are treated with vestibular neurectomy, Ménière’s disease and partial vestibular injury (viral or traumatic). The vestibular nerve itself is the superior half of CN VIII and can be slightly grayer in color than the cochlear division. It is important to divide the vestibular portion from the cochlear portion to maintain a patient’s ability to hear. As the facial nerve lies near, it is often desirable to have electromyographic (EMG) monitoring of

the facial nerve during surgery to avoid any indirect damage.43

Surgical Approaches

Surgical approaches for vestibular neurectomy include a retrolabyrinthine, retrosigmoid, and middle fossa approaches.43

18.4.2  Ménière’s Disease Clinical

Ménière’s disease is described clinically as recurrent attacks of vertigo (typically lasting 20 minutes up to hours), unilateral hearing loss, ear fullness, and tinnitus. The diagnostic criteria for definite Ménière’s disease include two or more episodes of vertigo, documentation of lowto medium-fre- quency hearing loss, fluctuating aural symptoms, and that other causes have been ruled out or are less likely. It is likely due to a process known as endolymph hydrops in which transient fluctuation occur where perilymph enters the endolymph space leading to swelling and organ dysfunction.44

Epidemiology

The prevalence of Ménière’s disease is about 1 in 150,000 people and affects both men and women in similar numbers, with the peak incidence between 40 and 60 years.44

Diagnostic Studies

Imaging with MRI to rule out underlying mass. Audiography should be pursued, to see if there is associated, and often transient, lowor medium-frequency sensorineural hearing loss. Further testing by specialists with videonystagmography can be completed as well and vestibular-evoked potentials are an option as well.44

Treatment

Nonsurgical

During acute attacks, a patient’s vertiginous symptoms can be managed with a variety of vestibular suppressing medications which include, but not limited to, antihistamines (like meclizine), phenothiazines, benzodiazepines, antiemetics (like metoclopramide or ondansetron), and topical anticholinergics (like scopolamine). Prevention of further attacks is managed with a low-sodium diet (1,500 mg/d) and often the addition of thiazide diuretics. Betahistine, a potent H3 receptor antagonist, may have a role in longterm management. There are no high-quality randomized clinical trials regarding the long-term treatments described above.44,​45

Surgical

For patient who are unable to manage with medical therapies or diet changes alone, surgical treatment is the next step. There are a variety of treatment options ranging from intratympanic corticosteroid injections, use of gentamycin, and even endolymphatic shunt procedures. For patients who do not respond, vestibular neurectomy or labyrinthectomy can be attempted. Labyrinthectomy should only be pursued if the patient is already deaf in the affected ear.44

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18.4.3  Facial Nerve Palsy Localization

Facial nerve palsy is divided into two different types of lesions depending on the location of the lesion. The differentiation between the two comes down to the lesion involving the CN VII nucleus or peripheral nerve itself, leading to a lower motor neuron lesion and those proximal to the nucleus, leading to upper motor neuron type lesions. In general, upper motor neuron lesions spare the forehead causing only mild orbicularis oculi weakness, whereas lower motor lesions affect the entire half of the face.46,​47

Etiology

The differential diagnosis is quite broad for a facial nerve palsy and a good way to break up the differential is sources of dysfunction leading to central or peripheral palsy. The differential for central CN VII palsy includes, but is not limited to, strokes, tumors, demyelination, and CNS infection (including abscess). The differential for peripheral CN VII palsy includes Bell’s palsy, demyelination, stroke, neoplasms (both intraand extracranial), trauma, congenital, iatrogenic, meningitis (which could be bacterial/fungal/viral/ noninfectious), inflammatory disorders, infiltrative diseases, myopathies, and neuromuscular junction disorders.46

Bell’s Palsy

Bell’s palsy is a subtype of an idiopathic facial nerve palsy with an acute (< 72 hours) onset of unilateral peripheral facial nerve weakness for which no specific etiology is uncovered. In the case, where a specific etiology is discovered, infectious or otherwise, this no longer becomes a Bell’s