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

•1920: William T. Bovie, a plant physiologist, invented his famous electrocoagulator, which used electric current to produce focused intense heat. Cushing applied this invention to his surgical practice in 1927 ( Fig. 2.4).21,​22

•1921: Jean-Athanase Sicard injected a contrast dye, lipiodol, into the CSF areas as Dandy had done with air, which was then followed by an X-ray. His experiments produced the first myelogram­ ( Fig. 2.9). Carl Nylén also designed and built the

Fig. 2.8  Pneumoencephalography and pneumoventriculography pioneered by Walter Dandy. (Reproduced, with permission, from Rover RL, et al, Progressive ventricular dilation following pneumoencephalography: a radiological sign of occult hydrocephalus, JNS. 1972;36(1):50-59.)

world’s first surgical microscope in this year, which he used for the first time for a case of chronic otitis media. It was upgraded from monocular to binocular in 1922 by Gunnar Holmgren, a Swedish otolaryngologist.23

•1924: Hans Berger develops the electroencephalogram (EEG), building on the work of Fritsch and Hetzig. He first used his EEG during a neurosurgical operation on a 17-year-old boy by Nikolai Guleke.24

•1927: A. Egas Moniz adapted the previous two techniques from Dandy and

­Sicard to intracranial vasculature, thus inventing cerebral arteriography ( Fig. 2.10).

•1944: Franc Ingraham and Orville Bailey discover the hemostatic utility of fibrin foam, a product prepared by fractionation of human plasma, and the duralike nature of fibrin film. Cohn and colleagues were simultaneously working on a similar product made from fractionated plasma called Gelfoam.25,​26

Fig. 2.10  Moniz’s cerebral arteriography adapted from Dandy and Sicard’s techniques for visualization of cranial and spinal cerebrospinal fluid spaces.

(Reproduced, with permission, from Lobo Antunes, J. Egas Moniz and cerebral angiography, J Neurosurg. 1974;40:427–32.)

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•1947: Speigel and Wycis report the first human use of a stereotactic apparatus to target intracranial lesions, laying the foundation for frame-based stereotactic brain biopsies.27

•1951: Lars Leksell coins the term “stereotactic radiosurgery”28 and thereafter develops the first Gamma Knife in 1967 for the treatment of trigeminal neuralgia.

•1953: Paul Harrington develops his rod system for posterior spinal fixation and fusion.

•1955: Leonard Malis develops bipolar coagulation by using fine-tip jeweler’s forceps.29

•1957: Theodore Kurze became the first neurosurgeon to use a microscope during surgery.

•1960s: A revolution was underway in neurosurgery with the microscope at its center. Contributors to its development included R.M.P. Donaghy, Julius Jacobson,­ Ernesto Suarez, M.G. Yasargil, and Harold Buncke, a plastic surgeon. Jacobson­ was also the leader in early microsurgical­ instrumentation, credited with creating the original microneedle holder and microscissors.

•1970s–1980s: The advent of computed tomography (CT) in the early 1970s and the emergence of magnetic resonance imaging (MRI) in the later 1970s provided­ the ability to visualize the brain and gave neurosurgeons the opportunity to target tumors or perform functional lesions to restore function. The first CT and first MRI applied to patients were in 1971 and 1977 respectively.30

•1988: L. Dade Lunsford installs the first Gamma Knife in the United States.31 Gamma Knife offers noninvasive alternative­ treatment for a variety of intracranial targets.

•1990s: Ken Winston and Wendell Lutz adapt radiosurgery to linear accelera-

tors, later redesigned and dedicated to radiosurgery and fractionated stereotactic radiotherapy.32 Mark Carol invents intensity­ modulation, allowing for three dimensional shaping of radiation.33

•2000s: The rod-lens endoscope is refined and coupled to minimally invasive image-guided approaches to the parasellar region, lowering morbidity and length of hospital stay for tumors previously requiring lengthy transcranial microneurosurgical dissection with significant postoperative morbidities and prolonged hospitalizations.

Pearls

•Among the titans of neurosurgery before the modern era, Horsley, Macewen, and Cushing are the key contributors to remember.

•Prior to the late 1800s, neurosurgery advanced little and was limited to the simple technique of trephining for cranial access. Spine surgery was almost out of the question, given the rates of infection.

References

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[2]Gross C. A hole in the head. Neuroscientist. 1999; 5(4):263–269

[3]El Gindi S. Neurosurgery in Egypt: past, present, and future-from pyramids to radiosurgery. Neurosurgery. 2002; 51(3):789–795, discussion 795–796

[4]Calvert CA. The development of neurosurgery. Lancet. 1946; 248(6434):918

[5]Maroon JC. Skull base surgery: past, present, and future trends. Neurosurg Focus. 2005; 19(1):E1

[6]Pascual JM, Prieto R, Mazzarello P. Sir Victor Horsley: pioneer craniopharyngioma surgeon. J Neurosurg. 2015; 123(1):39–51

[8]Preul MC. History of brain tumor surgery. Neurosurg Focus. 2005; 18:1–4

[9]Bliss M. Harvey Cushing: A Life in Surgery. New York, NY: Oxford University Press; 2012:170–171

[10]Horrax G. Some of Harvey Cushing’s contributions to neurological surgery. J Neurosurg. 1981; 54(4):436–447

[11]Surbeck W, Stienen MN, Hildebrandt G. Emil Theodor Kocher: valve surgery for epilepsy. Epilepsia. 2012; 53(12):2099–2103

[12]Greenblatt SH, Dagi TF, Epstein MH. A history of neurosurgery in its scientific and professional con- texts. Park Ridge, IL: American Association of Neurological Surgeons; 1997

[13]Knoeller SM, Seifried C. Historical perspective: history of spinal surgery. Spine. 2000; 25(21):2838– 2843

[14]Mohan AL, Das K. History of surgery for the correction of spinal deformity. Neurosurg Focus. 2003; 14(1):e1

[15]Singh H, Rahimi SY, Yeh DJ, Floyd D. History of posterior thoracic instrumentation. Neurosurg Focus. 2004; 16(1):E11

[16]Vaccaro AR. Fractures of the cervical, lumbar, and thoracic spine. Boca Raton, FL: CRC Press; 2002

[17]Kabins MB, Weinstein JN. The history of vertebral screw and pedicle screw fixation. Iowa Orthop J.

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[18]Gupta G, Prestigiacomo CJ. From sealing wax to bone wax: predecessors to Horsley’s development. Neurosurg Focus. 2007; 23(1):E16

[19]Goodrich JT. A millennium review of skull base surgery. Childs Nerv Syst. 2000; 16(10–11):669–685

[20]Lichterman B. The factors of emergence of neurosurgery as a clinical specialty. Hist Med. 2014; 2(2):37–51

[21]de Divitiis E. Development of instrumentation in neurosurgery. World Neurosurg. 2011; 75(1):12–13

[22]O’Connor JL, Bloom DA. William T. Bovie and electrosurgery. Surgery. 1996; 119(4):390–396

[23]Kriss TC, Kriss VM. History of the operating microscope:­ from magnifying glass to microneurosurgery. Neurosurgery. 1998; 42(4):899–907

[24]Tudor M, Tudor L, Tudor KI. Hans Berger (1873– 1941): the history of electroencephalography Acta Med Croatica. 2005; 59(4):307–313

[25]Ingraham F, Bailey O, Nulsen F. Studies on fibrin foam as a hemostatic agent in neurosurgery, with special reference to its comparison with muscle. J Neurosurg. 1944; 3:171–181

[26]Sachs E. The most important steps in the development of neurological surgery. Yale J Biol Med. 1955; 28(3–4):444–450

[27]Spiegel EA, Wycis HT, Marks M, Lee AJ. Stereotaxic apparatus for operations on the human brain. Science­ . 1947; 106(2754):349–350

[28]Leksell L. The stereotaxic method and radiosurgery of the brain. Acta Chir Scand. 1951; 102(4):­316– 319

[29]Yaşargil MG. Personal considerations on the his- tory of microneurosurgery. J Neurosurg. 2010; 112(6):1163–1175

[30]Edelman RR. The history of MR imaging as seen through the pages of Radiology. Radiology. 2014; 273(2):S181–S200

[31]Lunsford LD, Flickinger J, Lindner G, Maitz A. Ste- reotactic radiosurgery of the brain using the first

United States 201 cobalt-60 source gamma knife. Neurosurgery. 1989; 24(2):151–159

[32]Winston KR, Lutz W. Linear accelerator as a neurosurgical­ tool for stereotactic radiosurgery. Neurosurgery. 1988; 22(3):454–464

[33]Carol M, Grant WH, III, Pavord D, et al. Initial clinical experience with the Peacock intensity modulation of a 3-D conformal radiation therapy system. Stereotact­ Funct Neurosurg. 1996; 66(1–3):30–34

3.1  Introduction

Historically, the neurological examination was the primary method by which neurosurgeons evaluated a patient’s neurologic status, determined anatomic sites of dysfunction, and deduced the underlying pathology. Today, however, outpatients often arrive at the clinic with laboratory testing, electrophysiological studies, imaging, prior evaluation by a neurologist or primary care provider, and even an established diagnosis. Thus, in practice, neurosurgeons use a focused and selective neurological examination to corroborate pathology identified by other diagnostic modalities and assess the functional status of the patient. Similarly, for inpatients, the neurological examination is a rapid and cost-effective first-line assessment for tracking patient progress and assessing acute changes. This chapter summarizes key elements of the neurological examination.

3.2  Mental Status

This chapter offers a brief overview of the mental status examination (MSE), which is an important tool in assessing functional and cognitive deficits ( Table 3.1). This can be important in evaluating a patient with dementia; and from a neurosurgical perspective, the MSE may help localize a lesion to cortical regions of the cerebral cortex (frontal, parietal, temporal, and occipital lobes), which are regions of higher cognitive function. Importantly, if level of consciousness ( Table 3.2) and language ( Table 3.3) are not intact, other elements of the MSE cannot be accurately assessed.

3.3  Cranial Nerves

The integrity of a cranial nerve (CN) can be determined by quickly assessing its respective function ( Table 3.4).

3.3.1  CN I

CN I is rarely tested in clinical practice, but can be tested by having the patient identify common odors in one nostril at a time (e.g., coffee, vanilla).

3.3.2  CNs II and III

The examiner should have the patient cover one eye at a time while covering his or her own contralateral eye. The examiner should then hold up some fingers in the most peripheral areas of the visual fields and ask the patient to identify how many fingers are held up. Monocular vision loss localizes anterior to the chiasm, bitemporal hemianopia localizes to the crossing fibers of the chiasm, and homonymous hemianopia/quadrantanopia localizes posterior to the chiasm (seeFig. 18.1). Acuity can be tested using a hand-held visual acuity card one eye at a time.

Funduscopic Examination

The funduscopic examination is performed using an ophthalmoscope in darkness and ideally with the patient’s pupil dilated. One should generally observe a red reflex ­(reddish-orange reflection off retina), the margins and size of the optic disc, retinal vessel abnormalities, and retinal lesions (e.g., hemorrhages, exudates).

Pupillary Light Reflex

The pupillary light reflex simultaneously tests CNs II and III, as CN II senses incoming light and parasympathetic fibers running along the outside of CN III stimulates the pupillary constriction both in the ipsilateral eye (direct reflex) and in the contralateral eye (consensual reflex). The examiner should shine light directly onto one eye and observe whether both pupils constrict equally, and then test the other eye in the same manner. If the examiner swings the penlight back and forth between eyes, and one pupil is ­consistently larger than the other, this

suggests an afferent pupillary defect (APD) whereby CN II of the eye with the larger pupil is not intact.

3.3.3  CNs III, IV, and VI Eye Movements

The examiner should first observe for any ptosis, eye deviation, and nystagmus (involuntary eye movements) at baseline. Then, the examiner should have the patient follow his or her finger to make an “H” in space and observe if either eye is unable to fully move in a particular direction or if any nystagmus is elicited.

Classic nerve palsies include CN III palsy (“down and out”) in which the affected eye cannot be raised or adducted, CN VI palsy in which the affected eye cannot be abducted, and CN IV palsy in which the affected eye cannot look “in and down” (e.g., going down stairs, reading a book). Another classic finding is an internuclear ophthalmoplegia (INO) as a result of medial longitudinal fasciculus (MLF) damage in which the affected ipsilateral eye cannot adduct when it attempts to gaze contralateral relative to the affected eye.

Vestibulo-ocular Reflex

The vestibulo-ocular reflex (VOR) assesses the integrity of both CN VIII and two nerves that control extraocular muscles (CNs III and VI) simultaneously because activation of the vestibular system through head movement in one direction produces eye movement in the other direction, thereby enabling the eyes to remain fixed on a target. The VOR can also be elicited via cold-caloric testing, especially during a brain death examination, which mimics head movement away from the ear in which cold water is infused. Intact brainstem function is indicated by eyes moving toward the ipsilateral ear, while intact cortical function is indicated by contralateral horizontal nystagmus. It should be noted that if voluntary eye movement is impaired, but the VOR is intact, this points to a supranuclear gaze palsy stemming from a lesion above the brainstem.

3.3.4  CN V Facial Sensation

Facial sensation can initially be tested using light touch or pinprick testing on the

patient’s forehead (V1 ophthalmic division), cheeks (V2 maxillary division), and chin (V3 mandibular division). The examiner should have the patient close both eyes and ask if light touch or pinprick feels the same on both sides and probe for any pain, paresthesias, or numbness in each of the three divisions.

Muscles of Mastication

To test the muscles of mastication, the examiner should have the patient open the jaw and close the jaw against resistance as well as move the chin laterally on both sides.

3.3.5  CN VII Facial Strength

Facial strength can easily be assessed by having the patient shut the eyes tightly, smile, and puff out the cheeks. The examiner can also observe more subtle signs of facial weakness such as mild facial droop, nasolabial fold flattening, drooling, or dysarthria. With regards to CN VII, a central lesion will affect the contralateral lower half of the face but spare the forehead, whereas a peripheral lesion will affect the entire ipsilateral face.

Blink-to-Threat

Blink-to-threat is generally reserved for the patient with depressed consciousness or aphasia. It simultaneously tests CNs II and VII, as CN II transmits visual information from a threat, whereas CN VII controls blinking. The examiner should flick his or her fingers near the lateral edge of each eye and observe for blinking, being careful not to stimulate the corneal reflex (CNs V and VII) with excessive air movement or actually touching the cornea.

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3.3.6  CN VIII Vestibular Function

The VOR via head movement and coldcaloric testing can be assessed to evaluate the integrity of CN VIII. The presence of nystagmus that suppresses with visual fixation and is not direction-changing also suggests a peripheral CN VIII lesion that is affecting vestibular function.

Hearing Function

The examiner can grossly assess hearing by rubbing his or her fingers together close to the patient’s ear while the patient’s eyes are closed. The Weber and Rinne tests using a 512 Hz tuning fork may provide a more detailed assessment to distinguish between sensorineural and conductive hearing loss.

3.3.7  CN XI

Strength of the sternocleidomastoid is tested by asking the patient to rotate the head against resistance (hand pushing on chin). Strength of the trapezius is tested by asking the patient to shrug the shoulders against resistance (hands pushing on shoulders).

3.3.8  CNs IX, X, and XII Palatal Movement

The examiner should instruct the patient to open the mouth and say “ahhh”, observing for symmetric upward movement of the palate as well as the absence of uvula deviation. A CN X lesion may result in contralateral uvula deviation.

Gag Reflex

If the examiner requires more information, a gag reflex can be performed to simultaneously assess CNs IX and X, whereby the

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response to stimulating the oropharynx with a cotton swab on either side is compared.

Tongue Movement

The patient should protrude the tongue and move it laterally in both directions as well as superiorly and inferiorly. In addition, the examiner should have the patient push the tongue against the inside of the cheek on both sides with resistance from the examiner pushing on the outside of the cheek. A CN XII lesion may result in ipsilateral tongue deviation.

Dysarthria

Lesions of these nerves may result in dysarthria, which is a disorder of speech production rather than language. Verbal articulation may be tested with the following phrases: “no ifs, ands, or buts”, “baseball player”, and “fifty-fifty.”

3.4  Motor Examination

3.4.1  Bulk

The motor examination should begin with an inspection of muscle bulk, looking for symmetry, atrophy, and fasciculations, which are random, spontaneous, and involuntary muscle twitches.

3.4.2  Tone

Muscle tone refers to residual tension in a relaxed muscle, which often manifests as the resistance to passive stretch in a relaxed muscle. In order to accurately assess tone, the patient must relax the muscles and allow the examiner to move them passively.

Hypertonia is further described as spastic or rigid. Spasticity is seen when a