Spasm, pain, numbness—irritation. Paresis, paralysis, anæsthesia (constant)—destructive lesions. Both combined—variable symptoms, recurrent. Definite, fixed symptoms—structural lesions, usually progressive. Symptoms, variable as to place, time, subsidence and recurrence—functional lesions. Brain lesions. Pressure on brain—pain, spasm, nausea, dullness, blindness, stupor, coma, palsy. Congestion and anæmia synchronous. Lesions of cortex. Encephalic lesions—hemiplegia, with spasms, increased reflexes, spasms follow cranial nerves, vertigo, apoplexy, epilepsy, dementia, coma, little muscular atrophy, or dermal sloughing. Spinal lesions, paraplegia without spasm, reflex reduced or nil, follow spinal nerves, head symptoms less, much muscular atrophy, bed sores. Sensory and motor tracts, in crus cerebri, respiratory centres—inspiratory expiratory, inhibition. Salivation, sneezing, coughing, sucking, chewing, swallowing, vomiting. Cardiac centres, accelerating and inhibitory. Vaso-motor centre. Spasm centre. Perspiratory centre. Pons. Corpora quadrigemini, crura cerebri. Thalamus, corpus striatum. Cerebellum. Cerebral cortex: in ass; in dog. Spinal lesions: lateral half section: central anteroposterior, vertical section: superior columns: inferior columns: cervical lateral columns: respiratory tract: glycogenic centre: pupillary dilator: cardiac accelerator; vaso-motor, sudoriparous: centre for anal sphincter: for vesical sphincter: genital centre: vaso-motor and trophic centres: muscular sense tract: superior column and Goll’s. Table of phenomena from cord lesions.

In Irritation of nervous organs the symptoms (spasm, pain, numbness) are usually intermittent.

In Destructive Lesions of nervous organs the symptoms (paresis, paralysis, anæsthesia) are usually constant.

When irritation and destruction are associated the symptoms are variable and frequent. The characteristic symptoms of the two may coexist or succeed each other.

Structural Nervous Lesions have symptoms that are definite in their area of distribution, nature (spasm, paralysis) and permanency. Objective Symptoms predominate and the case is likely to be progressive and fatal.

Functional Nervous Diseases have symptoms of indefinite distribution, variable in character, with intermissions and spontaneous disappearances (as under marked excitement) and subjective symptoms predominate. They may, however, last for a length of time without change.

Localisation of Brain Lesions.

Lesions of the cranial nerves and their superficial and deep centres of origin need not here occupy attention. These may be studied in works on anatomy and physiology. Attention may be drawn rather to the remoter effects of ganglia which affect or control distant action, and to general pressure on the encephalon.

General Pressure on the Encephalon, whether through fracture of the cranium and depression of bone, by acute congestion, by blood extravasation, by inflammatory exudation, or by acute abscess, will cause pain, spasms, nausea, dullness, blindness, stupor and coma. After expulsion of the cerebro-spinal fluid from the cranial cavity, the increasing pressure compresses the blood vessels, reduces or interrupts the circulation and abolishes the functions in the parts deprived of blood. Thus congestion of one portion of the encephalon is usually associated with diminished circulation in another portion. Disorder in the first may occur from hyperæmia and irritation and in another part from a consequent anæmia.

Destructive Lesions of Cortex of One Cerebral Hemisphere may or may not cause permanent symptoms, as shown by the passage of a crowbar through the front of the left hemisphere, yet the man survived for 13 years and showed no loss of intelligence, his disposition and character alone having changed for the worse. The one hemisphere may by itself sufficiently control mental acts, while the other lies dormant or may even have undergone degeneration.

Diagnosis of Encephalic and Spinal Lesions. The following may be taken as guiding principles:

Encephalic: Hemiplegic or bilaterally hemiplegic grouping of symptoms.

Spinal: Paraplegic grouping of symptoms.

Encephalic: Frequent contracture or spasms of paretic muscles.

Spinal: Paralysis more perfect and continuous.

Encephalic: Reflexes in affected muscles increased: Cerebral inhibition absent.

Spinal: Reflex abolished or reduced in parts the seat of the lesion.

Encephalic: Spasms in areas of distribution of cranial nerves (not spinal.)

Spinal: Spasms and paralysis follow distribution of spinal nerves.

Encephalic: Head symptoms frequent (vertigo, apoplexy, epilepsy, dementia, coma).

Spinal: Relative absence of head symptoms.

Encephalic: Comparative absence of marked muscle atrophy.

Spinal: Atrophy in special muscular groups.

Encephalic: Little tendency to form bed sores.

Spinal: Tendency to form sloughs and bed sores.

Sensory (Æsthesodic) and Motor (Kinesodic) Tracts in Encephalon.

In the crus and above, the sensory tract lies dorso-laterad of the motor tract, forming about one-fifth of the crus, and extending upward through a white layer bending inward to form an angle and finally diverging to the different cortical convolutions. The motor tract is mainly contained in the inferior pyramids of the bulb, and constitutes the median two fifths and basal two fifths of the crus. Without entering farther into this subject it will be observed that lesions of the outer layer of the crus and its radiating fibres may cause hemianæsthesia of body or head, including the eye, while lesions of the median and basal layers and radiating fibres induce hemiplegia of the head, tongue, fore limb, hind limb, trunk, etc.

Respiratory Centres, Inspiratory and Expiratory are in the floor of the fourth ventricle between the centres for the vagus and accessory nerves, and are directly stimulated by the CO₂ in the blood. Secondary subsidiary centres are in the optic thalamus, in the corpora quadrigemini both anterior and posterior pairs, and finally in the cervical spinal cord, so that disorder of respiration may occur from lesions in these points as well as in the main oblongata centre.

Respiratory Inhibition and arrest depend on the vagus, the superior and inferior laryngeal nerves.

The Salivation Centre also lies in the floor of the fourth ventricle and stimulation of the medulla causes free secretion.

The Centres for Sneezing, Coughing, Sucking, Chewing, Swallowing and Vomiting are also seated in the oblongata, so that any one of these phenomena may come from a central irritation. In bulbar paralysis the loss of power usually extends from the tongue through the lips, cheeks, jaws, pharynx, larynx, to the respiratory muscles and heart. Coughing may be roused by irritation of the external auditory meatus, liver, stomach, bowels, or generative organs as well as from the air passages.

Cardiac Accelerating and Inhibiting Centres are both present in the bulb, the latter receiving its afferent impulse mainly through the vagus nerve. Stimulation of the vagi, anæmia of the bulb through decapitation or through tying both carotids, hyperæmia through tying of the jugulars, a venous state of the blood, and blows on the abdomen all slow or arrest the heart action. Digitalis or muscarin has a similar effect. The heart action is accelerated by febrile and inflammatory affections, by a high or low temperature by section of the vagi, by sipping of cold water, by atropine or curari, and by salts of soda. Potash salts on the other hand restore the inhibitory action of the vagi and lower the heart’s action.

The Vaso-Motor Center is also in the oblongata and the contraction of the vessels with increase of arterial pressure may ensue from afferent currents in the sympathetic nerve and many sensory trunks. The varying activity is seen in blushing, in the congestion of mucous membranes under rage or excitement, in the capillary contraction in the early stage of inflammation, in the second stage of capillary dilation, in angioma or nævus and in extensive congestions and hæmorrhages in different organs. The arrest of bleeding under fainting is due largely to the anæmia of this centre.

A Spasm Centre the pricking of which causes general convulsions lies in the medulla oblongata at its junction with the pons. This is excited by excess of carbon dioxide in the blood, by suffocation, drowning, by anæmia of the bulb from bleeding or ligature of the carotids, by venous congestion after ligature of the jugulars, or by the direct application to the part of ammonia carbonate, or salts of potash or soda. It may also be roused by afferent nervous currents from different peripheral parts (spinal cord, sciatic nerve, etc.).

A Perspiratory Centre is found in the medulla, on each side, which may be roused into action by diaphoretics (opium, ipecacuan, tartar emetic, Calabar bean, nicotin, picrotoxin, camphor, pilocarpin, ammonia acetate, etc.).

The Pons like the medulla is at once a ganglionic and conducting organ, and its lesions may lead to arrest of nerve currents generated above or below it, or to the failure to develop currents in its own centres. Stimulation of its superficial layers may be without effect, but if this is carried into the centre epileptiform convulsions ensue. Lesions of one side of its posterior half cause facial paralysis on the same side and motor and sensory paralysis on the opposite side of the body (crossed hemiplegia). Lesions of one side of its anterior half cause paralysis in both face and body on the same side. This depends on the crossing of the fibres midway back in the pons, which cross again in the medulla (motor fibres) and in the spinal cord (sensory fibres). Lesions of the pons are liable to interfere with the functions of the trigemini, the oculo motor and the superior oblique, and to determine epileptic movements and loss of coördination of sensorio-motor movements. Lesions of the superficial transverse fibres (median cerebellar peduncles) tend to cause involuntary movements to one side.

Lesions of the Corpora Quadrigemina cause disturbance of vision, failure of the pupil to contract to light, blindness, paralysis of the oculo-motor nerves, and lack of coördination of movements. Stimulation of one anterior corpus causes rolling of both eyes to the opposite side, with, if continued, a similar movement of the head and even of the body (horse in mill, or index motion, or rolling on its axis).

The Crura Cerebri are conducting bodies but contain also different nerve centres. Lesions of one crus cause violent pain and spasm on the opposite side of the body, followed by paralysis. The oculo motor may be paralyzed on the same side, but the face and tongue on the opposite side, owing to the fibres crossing in the pons. There may be turning movements.

The Optic Thalamus transmits sensory currents to the cerebral cortex. Lesions in this organ cause sensory paralysis on the opposite side of the body. Afferent currents that do not traverse the thalamus cause reflexes only. It contains one of the roots of the optic nerve and its destruction will impair vision. Its injuries may also produce turning movements.

The Corpus Striatum transmits motor currents originating in the cerebral cortex. Lesions of its interior (lenticular nucleus) cause motor paralysis and sometimes anæsthesia on the opposite side of the body. Electrical stimulation of this nucleus causes general muscular contractions of the opposite side of the body. Irritation of the surface layers is painless and symptomless.

The Cerebellum has been long credited with coördination, and Flourens, after its removal from a pigeon, found an utter lack of harmonized movement in walking, springing or balancing. Luciani removed the organ from a bitch and, after full healing of the part, found a lack of muscular tone (a cerebellar ataxy), so that no great muscular effort could be satisfactorily accomplished. After months, marasmus set in and proved fatal. The lack of coördination is especially connected with lesions of the vermiform process, those of the posterior portion causing falling forward and those of the anterior portion, falling backward. Injury to the middle peduncle on one side causes turning or rolling to the opposite side. Under slighter injuries there may be only unsteadiness and staggering like a drunken man. Nausea and vomiting, with more or less stiffness of the neck or oposthotonos, may be present. Rolling of the eyes or squinting may occur.

Focal Cortical Centers of the Cerebrum. Cortical Localization. Much has been done experimentally and by observation of morbid lesions to locate functions in the different convolutions, and though the subsidiary implication of adjacent and interdependent parts interferes with a perfectly confident diagnosis, yet certain fundamental facts may be borne in mind as contributing to a satisfactory diagnosis.

Arloing, on the basis of his own experiments and those of his predecessors, gives the following as applicable to the equine (ass) brain:

1. Stimulation of the origin of the front part of the first frontal convolution, or of the anterior part of the pre-Sylvian convolution, causes approximation of the feet on the opposite side of the body.

2. Stimulation of the superior part of the first frontal convolution or of the superior part of the post-Rolandic convolution causes closure of the jaws and diduction.

3. Stimulation of the anterior end of the upper orbital convolution, or of the anterior part of the pre-Rolandic convolution, leads to movements of the nose and upper lip.

4. Stimulation of the antero-superior part of the lower frontal convolution, or the union of the post-Rolandic with the Sylvian convolution causes movement of tongue and jaws.

5. Stimulation of the union of the vertical and horizontal parts of the orbital convolution or frontal lobe, causes opening of the jaws and bending of head and neck.

6. Stimulation in the front of the union of the frontal and longitudinal convolutions, or at the union of the Sylvian and second parietal convolution causes rolling of the opposite eye.

7. Stimulation of union of the frontal and parietal parts of second parietal convolution leads to closure of both eyelids or, with a strong current, of lids on both sides.

8. Stimulation of the second parietal convolution, above and a little behind the extremity of the Sylvian fissure, causes opening of the eye and adduction of the ear on the opposite side, or, if a very strong current, on both sides.

9. Strong stimulation of the posterior part of the first and second parietal convolutions causes tonic convulsions.

10. Currents through the posterior parts of the third and fourth parietal convolutions gives similar convulsions with violent trembling of the trunk and members.

In the Dog’s Brain localization is easily made by reference to the crucial fissure which passes outward, right and left, at right angles with the longitudinal fissure about the junction of its anterior with its middle third. Also by four parietal convolutions which run backward from near the crucial fissure, parallel with the longitudinal fissure. They are counted from without inward. Fritsch, Hitzig and Ferrier have mapped out the following motor areas:

1. The convolution in front of the outer end of the crucial sulcus controls the muscles of the neck.

2. The bend of the same convolution backward, opposite the outer extremity of the crucial sulcus, controls the extensors and adductors of the fore limb.

3. The convolution just behind the outer end of the crucial sulcus controls the muscles which flex and rotate the fore limb.

4. The same convolution behind the middle of the crucial fissure controls the movements of the hind limb.

5. The second convolution back of the crucial fissure controls the muscles of the face.

6. The anterior part of the internal (4th) parietal convolution, just back of the crucial fissure, controls the lateral switching movements of the tail.

7. The posterior angle of the first post-crucial convolution causes retraction and abduction of the fore limb.

8. The outer end of the first post-crucial convolution, directly behind the outer end of the sulcus, causes raising of the shoulder and extension of the fore limb.

9. The anterior end of the third parietal convolution (the second from the longitudinal fissure) controls closure of the eyelids, the rolling of the eyeball upward, and narrowing of the pupil.

10. Stimulation of the anterior end of the second parietal convolution causes partial opening of the mouth with retraction and elevation of its angle.

11. Stimulation of the point of union of the first and second parietal convolutions anteriorly causes opening of the mouth with protrusion and retraction of the tongue.

12. Stimulation of the median part of the second parietal convolution, causes retraction and elevation of the angle of the mouth.

13. Stimulation of the convolution directly in front of the outer end of the crucial sulcus causes dilatation of the eyelids and pupil while the eyes and head are turned toward the opposite side.

14. Stimulation of the convolution behind the crucial fissure causes contraction of the muscles of the perineum.

15. Stimulation of the convolution in front of the crucial fissure, on its anterior and sloping portion, causes movements of the pharynx and larynx (swallowing).

16. Stimulation of motor areas of the cortex, by scraping, irritation, or disease tends to produce spasmodic contractions of certain groups of muscles (Jacksonian Epilepsy). Strong stimulation may cause general epileptiform spasms, which are at first tonic, then clonic. One such seizure strongly predisposes to a second. If, during an attack, the cortical centres presiding over a special group of muscles were sliced off, such muscles relaxed, though the general spasms in the other muscles continued.

Localizations of Spinal Lesions.

Being at once a conductor between the brain and nerves, and a reflex nerve centre, we must consider both rôles in seeking to locate lesions from symptoms. In passing from the nerves to and from the sensorium both sensory and motor currents cross so that one side of the brain presides over the other side of trunk and limbs. This crossing of the motor fibres takes place in the medulla oblongata, while that of the sensory fibres occurs in the spinal cord close in front of the nerve from which they have entered.

Cross-Section of one lateral half of the spinal cord therefore causes motor paralysis and rise of temperature of the whole of that side of the body posterior to the lesion, while it induces sensory paralysis and cooling on the opposite side of the body up to the same point. A very limited sensory paralysis on the same side occurs corresponding to the few sensory fibres passing outward obliquely through the portion injured by the cross-section.

A vertical section of the cord separating the one lateral half from the other does not necessarily affect the motor currents, while it produces a limited anæsthesia on each side in the area of distribution of the nerves, the sensory fibres of which crossed in the seat of the lesion.

Transverse section of the superior columns causes hyperæsthesia and lack of coördination.

Transverse section of inferior columns, or of the inferior horn of gray matter, if close behind the medulla, causes no motor paralysis, but if farther back induces motor paralysis on the same side of the body.

Transverse section of the cervical lateral columns causes motor paralysis of the lateral walls of the chest (respiratory tract). If the section is made in the dorsal or lumbar region it is the same as lesion of the superior columns.

Among reflex centres in the cord the following may be named:

The Respiratory Tract in the cervical lateral columns just referred to.

A Glycogenic Centre in the anterior cervical section between the bulb and the fourth cervical nerve.

Centres which Dilate the Pupil between the fifth cervical and the sixth dorsal nerve.

Cardiac Accelerator Centres between the three last cervical and the five first dorsal nerves.

Vaso-Motor Sudoriparous Centres in the central gray matter.

Centre for Anal Sphincter between the sixth and seventh dorsal nerves.

Centre for Vesical Sphincter between the third and fifth lumbar nerves.

Genital Centre, opposite the first lumbar nerve.

Vaso-motor and Trophic Centres are found in the inferior horns of gray matter, and their degeneration causes progressive muscular atrophy.

The Muscular Sense Tract is located near the surface of the superior columns, so that a certain amount of incoördination and unsteadiness of progression follows its destruction.

The Deeper Part of the Superior Columns and the Column of Goll which bounds the superior median fissure control muscular sense and coördination, and their disease (posterior lateral sclerosis) entails locomotor ataxy.