Cases Flashcards

cases location (40 cards)

1
Q

A dog:
1. Lossofproprioceptivepositioningandtactileplacingresponsesfrom both forelimbs.
2. Proprioceptivepositioningandtactileplacingresponsesnormalinboth hindlimbs.
3. Paralysisofthetonguewithbilateralatrophyoftheintrinsictongue muscles.

A

The bilateral loss of kinaesthesia from the forelimbs but not the hindlimbs is consistent with a lesion in the midline of the medulla oblongata in the dorsal part of the medial lemniscal system. The bilateral paralysis of the tongue indicates destruction of the motor nucleus of the hypoglossal nerve on both sides and confirms that the level of the lesion is in the caudal part of the medulla oblongata

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2
Q

A cat:
1. Completelossofresponsestotouchandproprioceptivepositioninginthe left forelimb and left hindlimb, and loss of responses to touch on the left side of the head.
2. Adductionoftherighteyeball.

A

The whole of the right medial lemniscal system is interrupted. The level is at the motor nucleus of the abducent nerve, at the rostral end of the medulla oblongata

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3
Q

A cat:
1. Completelossofresponsestotouchandproprioceptivepositioninginthe right forelimb and right hindlimb, and loss of responses to touch on the right side of the head.
2. Visualdeficitinthenasalfieldofthelefteyeandthetemporalfieldof the right eye.

A

A lesion in the left cerebral cortex

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4
Q

A dog:
1. Lossofthewithdrawalreflexfromtherightforelimb.
2. Lossofproprioceptivepositioningfromrightforelimb.
3. Lossofpanniculusreflexfromalloftherightside.
4. Proprioceptivepositioningisnormalinthelefthindlimb,buttheright hindlimb shows a slight proprioceptive deficit.
5. Withdrawalreflexesnormalinbothhindlimbs.
6. Distaltotherightshoulder,noresponsetopain,exceptforthelateral aspect of the brachium and the medial aspect of the antebrachium.

A

A lesion has affected the right dorsal roots and/or the right dorsal horn at segments C8 to T2 of the spinal cord. The hindlimb proprioceptive deficit suggests that the lesion may also have affected the gracile fascicle in the right dorsal funiculus. The loss of the panniculus reflex could be explained by involvement of the dorsal horn at C8 and T1, since the final ascending projections of this reflex must enter the grey matter at this level. The loss of the withdrawal reflex and the absence of pain response from the paw indicate that spinal nerves C8, T1, and T2 are involved, since the median, ulnar and radial nerves arise almost entirely from these spinal nerves. The presence of a pain response from the lateral aspect of the brachium and from the medial aspect of the antebrachium indicates that C7 is not involved, since this nerve is the main source of the axillary and musculocutaneous nerves. The lesion is unlikely to be peripheral, since there is both a hind‐ and forelimb deficit.

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5
Q

A dog:
1. Inordinarydaylight,theleftandrightpupilsareofnormaldiameter.
2. Thereisnostrabismus.
3. Lightdirectedintotherighteyeproducesbothadirectandaconsensual response.
4. Lightdirectedintothelefteyeproducesneitheradirectnoraconsensual response.
5. Menaceandvisualplacingresponsesnormalforrighteye,negativefor left eye.

A

The animal is blind in the left eye only, so the lesion is in the left optic nerve (or left retina)

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6
Q

A dog:
1. Inordinarydaylight,therightpupilisabnormallydilated.
2. Thereisnostrabismus.
3. Lightdirectedintotherighteyeproducesaconsensualresponsebutnota direct response.
4. Lightdirectedintothelefteyeproducesadirectresponsebutnota consensual response.
5. Visualplacing,menaceandfixatingresponsesnormalinbotheyes.

A

The optic nerve and optic tracts are normal, but the right parasympathetic oculomotor nucleus is destroyed. The lesion is in the midbrain (but the motor nucleus of the oculomotor nerve is normal, since there is no strabismus).

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7
Q

A dog:
1. Theownerreportsthattheanimalseemstobeabletoseeonlywhatis directly in front of it.
2. Examinationshowsthatthedogisblind,exceptforasmallpartofboth the left and the right nasal fields immediately adjacent to the midline.
3. Directandconsensualpupillaryreflexesnormalinbotheyes.

A

The loss of vision in one‐half of each visual field is called hemianopia. In this dog. the temporal half of the visual field of each eye is lost, constituting bitemporal hemianopia. Also lost is the adjoining part of the nasal half of the visual field of each eye, leaving intact only the most medial part of the nasal field. Since the animal can only see what is directly in front of it, the deficit can be described as ‘tunnel vision’. Only the decussating fibres have been damaged; in the dog these fibres account for 75% of the total optic pathway. A midline lesion of the optic chiasma, such as a pituitary tumour, could account for these visual defects (Figure 9.1). The pupillary reflexes are normal in both eyes, because the most lateral part of the retina of both eyes still responds normally to the light stimulus.

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8
Q

A horse:
1. Nystagmus,slowphasebeingtowardstheleft. 2. Tendencytofalltotheleft.
3. Leftfacialparalysis.
4. Headtilted,thelefteargoingdown.

A

A lesion in the left side of the medulla oblongata, involving the left vestibular nuclei and left motor nucleus of the facial nerve. Lesions in the middle and inner ear also could readily account for these signs. So also could compression of the roots of the left VIIth and VIIIth nerves by a tumour, as they arise from the brainstem.

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9
Q

A cat:
1. Avisualdeficitisobservedinthetemporalfieldofthelefteyeandinthe nasal field of the right eye.
2. Directandconsensualpupillaryreflexesarenormalinbotheyes.
3. Thereisaslightimpairmentofbalance,withoutclearemphasisoneither the left or right side of the body.
4. Theownerreportsageneralreductioninhearing.

A

A lesion in the right lateral and medial geniculate bodies

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10
Q

A dog:
1. Themenaceresponseisnegativeforboththeleftandtherighteyes.
2. Thevisualplacingresponseisnegativeforbotheyes.
3. Lightdirectedintothelefteyeproducesadirectandconsensualpupillary response. So does light directed into the right eye.
4. Thereishypertonusofthelimbsonbothsides.

A

The optic nerves, optic tracts and rostral colliculi are normal on both sides, since the pupillary reflexes are fully functional.
But there is complete blindness. This could mean destruction of the visual cortex on both sides. Alternatively, both lateral geniculate nuclei could be destroyed. The hypertonus of all limbs is consistent with destruction of motor areas of the cerebral cortex, and confirms the presence of widespread damage to the left and right cerebral cortex. Lesions and clinical signs of this type, termed cerebrocortical necrosis, have been recognised in the cat following cardiac arrest during anaesthesia and in ruminants suffering from thiamine deficiency.

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11
Q

A cat:
1. Difficultyinswallowing.
2. Lossofgagreflexonleftside.

A

Destruction of the left nucleus of the solitary tract could account for this case, since there is loss of all afferent information from the left side of the pharyngeal mucosa, travelling mainly in nerve IX and also in nerve X.

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12
Q

A cat:
1. Thetonguetendstoprotrudefromthemouth,deviatingtotheright. 2. Wastingoftherightsideofthetongue.

A

Destruction of the right motor nucleus of the hypoglossal nerve. This amounts to a lower motor neuron lesion, as shown by muscle wasting.

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13
Q

A dog:
1. Difficultyinswallowing.
2. Changeofvoice.
3. Rightvocalfoldpermanentlyadducted.

A

This combination suggests a deficit in the motor innervation of the pharynx and larynx (vagal branches), and could be due to a lesion of the right nucleus ambiguus

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14
Q

A horse:
1. Lefteyenormal.
2. Up‐and‐instrabismusofrighteye.

A

Up‐and‐in strabismus of the right eye indicates failure of the right dorsal oblique muscle, and hence of the motor nucleus of the trochlear nerve. Since the axons of this nucleus decussate, this lesion is in the left nucleus.

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15
Q

A dog:
1. Righteyenormal.
2. Downwardandoutwardstrabismusoflefteye.

A

The left dorsal oblique and lateral rectus muscles are still in a state of tone, unopposed by the paralysed ventral oblique and medial rectus muscles. The lesion is in the left motor nucleus of the oculomotor nerve.

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16
Q

A horse:
1. Lipsdrawntowardstheleftside. 2. Rightlowereyeliddrooping.
3. Righteardrooping.

A

A lesion of the right motor nucleus of the facial nerve.

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17
Q

A horse:
1. Dryingofrightcornea.
2. Dryingofnasalmucosaonrightside. 3. Reducedsalivationwhenfeeding.

A

A lesion of the right parasympathetic nucleus of the facial nerve, which distributes parasympathetic motor pathways through the trigeminal nerve to the lacrimal gland, glands of the nasal mucosa, and the submandibular and sublingual salivary glands

18
Q

A dog:
1. Diabetes insipidus.
2. Extremitiesandearsfeelcold. 3. Periodicshivering.
4. Lossofappetite.

A

A lesion in the hypothalamus, disturbing various autonomic functions

19
Q

A dog:
1. Flaccidparalysisofleftforelimb.
2. Totallossofwithdrawalreflexfromleftforelimb.
3. Somewastingoflefttricepsmuscle.
4. Leftforelimbwarmerthantheright.
5. Rightforelimbnormal.
6. Slightparesisoflefthindlimbwithexaggeratedreflexes. 7. Righthindlimbnormal.
8. Slowheartrate.

A

A lesion of the left side of the spinal cord at segments C6 to T2. Flaccid paralysis and muscle wasting are explicit signs of a lower motor neuron lesion. The total loss of all response to the withdrawal reflex means that all the flexor muscle groups and their nerves are involved, i.e. the axillary, musculocutaneous, median and ulnar nerves; the wasting of triceps shows that the radial nerve is also affected. Therefore, the lesion has taken out the left ventral horn of segments C6, C7, C8, T1 and T2 (forming the brachial plexus). The autonomic effects indicate involvement of the left lateral horns of segments T1 to T5. The lesion has also disturbed the white matter in the left lateral funiculus (e.g. it may have interrupted some or all of the left lateral corticospinal, left rubrospinal and left reticulospinal tracts), causing an upper motor neuron disorder of the left hindlimb (hyperreflexia).

20
Q

A sheep:
1. Continuouscirclingtotheleft.
2. Intermittentaversionofhead,theeargoingdownontherightside.
3. Blindfoldingofthelefteyecausesnochangeinpostureorlocomotion, but blindfolding of the right eye causes the animal to stagger and fall repeatedly to its left side.
4. Hemiwalkingtestsindicatealocomotorydeficitintheleftlimbs.

A

These signs suggest a unilateral cerebral cortical lesion (e.g. caused by a Coenurus cyst), but the question is, on which side is the lesion? The direction of circling and head aversion are not reliable indicators of the side. The relatively dramatic effect of blindfolding the right eye suggests that the animal has vision with this eye; the left eye is probably blind, and this is consistent with a right cerebral cortical lesion. The locomotory deficit that was revealed in the left limbs, by hemiwalking, strongly supports a right cerebral cortical lesion. The postural–locomotory deficit of the left limbs could be largely compensated by vision in the right eye. But blindfolding the

right eye renders the animal virtually blind; the postural–locomotory deficit of the left limbs then becomes unmanageable, so the animal falls to the left side. Conclusion: a large unilateral lesion in the right cerebral cortex.

21
Q

A cat:
1. Circlingtotheleft.
2. Occasionalfallingandrollingovertotheleftside.
3. Theleftsideofthefaceisconstantlytilteddownwards. 4. Visionisentirelynormalinbotheyes.

A

These signs indicate a destructive lesion of the left vestibular nuclei. The normal vision argues against an extensive lesion of the cerebral hemispheres.

22
Q

A dog:
1. Generalinsecurityofposture,withthelimbswideaparttomaintain balance when standing.
2. Hypertoniaofalllimbs.
3. Tremoroflimbs,accentuatedduringfinemovementslikeplacingthe paw on an object to restrain it.

A

These signs suggest a midline cerebellar lesion. The difficulty in maintaining balance indicates involvement of the vestibulocerebellum. The hypertonia suggests that the spinocerebellum is affected. The tremor reveals pontocerebellar involvement. Thus, all three cerebellar components are affected. There is no indication of unilateral deficits

23
Q

A dog:
1. Hypertonusofrightforelimb,theotherlimbsbeingnormal.
2. Intermittenttremorofrightforelimb,notincreasedduringmovementand disappearing during sleep.
3. Occasionalspontaneousexaggeratedandincoordinatedmovementsof the right forelimb.
4. Allafferentresponsesnormal.

A

Hypertonus, tremor, and particularly the spontaneous exaggerated movements on the right side, suggest a lesion somewhere in the left basal nuclei, the effects of such lesions being usually contralateral

24
Q

A horse:
1. Paresis(weakness)ofallfourlimbs.
2. Hyperreflexiaofallfourlimbs.
3. Stiffgait,suggestiveofhypertonus.
4. Defectiveproprioceptivepositioningresponsesfromthehindlimbson both sides.
5. Distressedbreathing(dyspnoea).
6. Allcranialnerveresponsesnormal.

A

The paresis, hyperreflexia and hypertonus are consistent with an upper motor neuron disorder resulting from a lesion of the white matter of the spinal cord (see Section 14.6). The proprioceptive deficit also suggests damage to the white matter of the spinal cord. Clinical signs like these can occur from very widespread and scattered lesions of the white matter on both sides of the cervical spinal cord, somewhere between C3 and C7 (as in the wobbler syndrome in the horse and dog). The greater involvement of the hindlimbs rather than the forelimbs is typical of the wobbler syndrome. The dorsal funiculus is only mildly affected in wobbler horses, so that a joint proprioceptive deficit is not obvious in the forelimb. But many of the proprioceptor pathways from the joints of the hindlimb have probably transferred from the gracile fascicle to the dorsal spinocerebellar tract in the dorsolateral part of the lateral funiculus (see Section 8.4). In wobblers, degeneration affects the dorsolateral part of the lateral funiculus, thereby involving both the joint proprioceptors from the hindlimbs and also the dorsal spinocerebellar tract from the hindlimb. Spinocerebellar fibres are now known to contribute to the sense of kinaesthesia (see Section 10.5). The dyspnoea may arise from disturbance of reticulospinal pathways, leading to erratic and inadequate operation of the diaphragm and intercostal muscles.

25
A dog: 1. Retentionanddribblingofurineandretentionoffaeces. 2. Perinealreflexandtailresponselost. 3. Thehindlimbsshowsevereparesis,incoordinationandhypotonus. 4. Withdrawalreflexalmostlostinbothhindlimbs. 5. Somewastingofpartsofthehamstringmusclesofbothlegs. 6. Lossofpainresponsefromtheskindistaltothestrifle,exceptthemedial aspect of leg and paw, of both hindlimbs. 7. Normalpainresponsesfromthecranialregionofleftandrightthigh. 8. Patellarreflexnormalinbothlimbs.
This could be a lesion which has extensively damaged both the grey and white matter of the spinal cord in segments L6 to S3 inclusive. Some of the lower motor neurons in the sciatic nerve (spinal nerves L6, L7, S1), as well as preganglionic neurons of the pelvic nerve (see Section 17.9), are involved. Since the patellar reflex is normal, the femoral nerve including the saphenous nerve, which is sensory to the medial aspect of the lower leg and paw), has escaped. The femoral nerve is formed mainly by spinal nerves L4 and 5. The cause could be a protrusion of the intervertebral disc at L4–5, affecting the spinal cord segments L6 to S3. Alternatively, there could be a massive compressive lesion (abscess, tumour, fracture) within the vertebral canal of vertebra L7, damaging the relevant nerves within the cauda equina (L7, S1, S2, S3).
26
A dog: 1. Paresisofbothhindlimbs. 2. Somewastingofvastusmusclesofbothlimbs. 3. Patellarreflexabsentinbothlimbs. 4. Normalpainresponsesfromtheskinofbothhindlimbs,includingthe cranial and medial aspects of the thigh. 5. Withdrawalreflexexaggeratedinbothhindlimbs. 6. Normalcontrolofurinationanddefecation. 7. Perinealreflexnormal.
The absence of the patellar reflex and the presence of muscle wasting in the vastus muscles indicate a lower motor neuron lesion, in this instance affecting the ventral horn on both sides of segments L4 and 5 of the spinal cord, thus destroying the motor outflow of the left and right femoral nerves. The presence of pain responses from the skin of the cranial and medial aspects of the thigh (conducted by the femoral nerve) shows that there is a central lesion, rather than peripheral damage to the femoral nerves. The exaggerated withdrawal reflex indicates that the white matter of the lateral and/or ventral funiculi has become involved, giving an upper motor neuron lesion of segments L6 and L7 of the spinal cord (sciatic nerve is L6, L7, and S1). However, pain pathways through the spinoreticular tracts in the lateral column have survived. Normal urination, defecation and perineal reflex indicate that the reticulospinal tracts and segments S1, S2 and S3 of the spinal cord have escaped. The cause could be a disc protrusion at disc L3–4, damaging spinal cord segments L3, L4 and L5.
27
A dog with: 1. Depressedmentalstatus. 2. Somestaringepisodes. 3. Absentmenaceresponsebilaterally. 4. Normalvision. 5. Cranialnervereflexesnormal. 6. Spinalreflexesnormal. 7. Proprioceptionnormalinallfourlimbs.
Diffuse forebrain lesion. MRI scans of the dog’s brain revealed bilateral asymmetrical intra‐axial lesions corresponding to the white and grey matter of both frontal lobes. No midline shift was visualised. The lesions revealed mild heterogeneous enhancement on the post contrast MR images. Cerebrospinal fluid analysis revealed a mild mononuclear pleocytosis. The final histopathological diagnosis was granulomatous meningoencephalitis. The lack of menace response in both eyes is likely to be due to damage of the anatomical pathway responsible for this response at the level of the motor cortex and internal capsule association/projection fibres.
28
A dog with progressive tetraparesis: 1. Alertandbright. 2. Cranialnervesnormal. 3. Menaceresponsenormalinbotheyes. 4. Non‐ambulatoryflaccidtetraparesis. 5. Proprioception is severely decreased in both hindlimbs and forelimbs. 6. Severeatrophyoftheappendicularmusclesoftheforelimbsand mild/moderate atrophy of the appendicular muscles in the hindlimbs. 7. Flexorreflexdecreasedinbothforelimbs. 8. Absentcutaneoustruncireflexbilaterally. 9. Hyperesthesiaduringdeeppalpationofthedog’scranialthoracic paraspinal muscles. 10. Nopainelicitedatmanipulationofthecervicalspine.
Spinal cord lesion C6/T2. MRI scans of the dog’s cranial thoracic spine showed a large mass‐like lesion invading the soft tissues and the bone tissues between T1 and T4 vertebral bodies. The lesion appeared to destroy and infiltrate the spinous processes of the vertebrae from T1 to T4. The lesion was also invading and severely compressing both sides of the spinal cord parenchyma at T1–T4. The MRI features were consistent with a neoplastic process having an aggressive progression. The final histopathological diagnosis was soft tissue sarcoma of intermediate grade. The paresis of both hindlimbs is caused by disruption of the UMN system, whereas the paresis of both forelimbs is of LMN origin as a consequence of the bilateral damage of the T1/T5 spinal cord segments with subsequent dysfunction of the median, radial and ulnar peripheral nerves. The loss of proprioception in all four limbs is caused by a dysfunction of the general proprioceptive afferent system at the cervicothoracic spinal cord segments. The decreased flexor reflex in both forelimbs is caused by the LMN dysfunction of the spinal cord/peripheral nerves at T1/T5 spinal cord segments. The cutaneous trunci reflex is absent bilaterally as a consequence of the dysfunction of the fasciculus proprius running in the lateral funiculus and/or the damage of the ventral grey column at C8/T1 and/or dysfunction of both lateral thoracic nerves. The atrophy of the appendicular muscles in the forelimbs is due to a combination of neurogenic and disuse muscle atrophy. The atrophy of the appendicular muscles in the hindlimbs is a disuse atrophy. The decreased flexor reflex in both hindlimbs is likely to be due to a decreased tone of the hindlimbs’ appendicular muscles.
29
A cat with progressive ambulatory paraparesis: 1. Brightandalert. 2. Cranialnervefunctionnormal. 3. Menaceresponsenormalinbotheyes. 4. Non‐ambulatoryspasticparaparesis. 5. Increasedpatellarreflexesinbothhindlimbs. 6. Cutaneoustruncireflexabsentontheleftsidecaudallytothe thoracolumbar spinal region and present on the right side. 7. Severehoppingandproprioceptivedeficitsinbothhindlimbs. 8. Deeppainperceptionpreservedinallfourlimbs. 9. Severehyperesthesiaelicitedonpalpationofthethoracolumbar paraspinal muscles. 10. Urinarybladderseverelyenlargedanddifficulttoexpressmanually.
Spinal cord lesion T3/L3. Radiographs of the cat’s thoracolumbar spinal region revealed moderate bone rarefaction/lysis at the L2 vertebral body, narrowing of L1/L2 intervertebral space and cloudiness of the intervertebral foramen at L1/L2. MRI scans of the cat’s thoracolumbar region revealed a well‐defined mass‐ like lesion invading the L2 vertebral body, left nerve root arising at L1/L2, epaxial and hypo‐axial muscles at the left cranial lumbar region. There was also left lateral compression of the spinal cord by the thickened nerve root. The histopathological diagnosis of the tru‐cut biopsies from the lesion was suggestive of an apocrine or sebaceous gland carcinoma from the dermal adnexae. The non‐ambulatory spastic paraparesis, together with bilateral increased patellar reflex, are classic neurological signs signifying a dysfunction of the UMN system. The proprioceptive deficits in both hindlimbs are caused by dysfunction of the general proprioceptive afferent system secondary to a lesion at T3/L3. The loss of the cutaneous trunci reflex at the left side indicates a spinal cord lesion mostly lateralised to the left and is caused by dysfunction of the left fasciculus proprius. The enlarged urinary bladder, which is difficult to express, is a consequence of the interruption of the cranially projecting sensory (GVA) and caudally projecting motor (UMN) pathways to the urinary bladder.
30
A cat with progressive paraparesis: 1. Brightandalert. 2. Cranialnervereflexesnormal. 3. Menaceresponseunremarkableinbotheyes. 4. Ambulatoryparaparesisandspinalhindlimbataxia. 5. Proprioceptivedeficitsinbothhindlimbs. 6. Normalspinalreflexesinallfourlimbs. 7. Cutaneoustruncireflexnormalbilaterally. 8. Hyperesthesiaatdeeppalpationoftheparaspinalmusclesorat manipulation of the cat’s cervical area.
Spinal cord T3/L3. MRI scans of the cat’s thoracolumbar region revealed a well‐defined mass‐ like lesion at the T11 vertebral body area invading the right nerve root, spinal cord, epaxial muscles and part of the dorsal portion of the pleural space. In addition, there was lysis of the caudal portion of T11 vertebral body. The lesion showed marked enhancement. The final histopathological diagnosis was a spindle cell sarcoma. The paraparesis and spinal hindlimb ataxia is caused by dysfunction of both the UMN system and general proprioceptive afferent system, respectively, secondary to a spinal cord lesion at T3/L3. The proprioceptive deficits in both hindlimbs are a consequence of the dysfunction of the general proprioceptive afferent system.
31
A dog with inability to close the left eye: 1. Alertandbright. 2. Gaitnormal. 3. Mildheadtilttowardstheleft. 4. Slightelevationoftheleftear,narrowedleftpalpebralfissure,theleft lips appear taut with the angle drawn caudally, the nose is slightly deviated toward the left side. 5. Palpebralreflexabsentinthelefteye. 6. Facialsensationispreserved. 7. Menaceresponsenormalinbotheyes. 8. Ventrolateralvestibularstrabismusinthelefteye. 9. Directandconsensualpupillarylightreflexesarenormal. 10. Proprioceptivepositioningnormalinallfourlegs. 11. Nohoppingdeficitsdetectedinanyofthedog’slimbs. 12. Noabnormalnystagmusobserved.
Left peripheral vestibular system and left facial nerve (left hemifacial spasm). At induction of general anaesthesia the left hemifacial spasm disappears. MRI scans of the dog’s brain are unremarkable, as well as the cerebrospinal fluid analysis. Electromyography (EMG) was carried out under general anaesthesia and showed continuous spontaneous motor unit discharges, mainly doublets in the left orbicularis oris/buccinator muscles. The EMG findings could indicate a defective glycinergic inhibition of the alpha‐motoneurons in the left facial nerve nucleus, which is a finding usually seen with tetanus. The imaging and electrophysiology testing support a diagnosis of left hemifacial spasm together with idiopathic left peripheral vestibular syndrome. The facial spasm on this dog remained permanent. Two weeks after presentation, the dog fully recovered from the left peripheral vestibular syndrome.
32
A dog presented with a history of slowly progressive generalised ataxia and head tilt towards the left: 1. Bright,alertandresponsive. 2. Vestibularataxiawithmildhypermetriaintherightforelegandright hindlimb. 3. Headtilttowardstheleft. 4. Proprioceptivedeficitsintherightforelegandrighthindlimb. 5. Cranialnerveexamination:unremarkable. 6. Normalmenaceresponseinbotheyes. 7. Spinalnervereflexes:normal. 8. Thereisnoabnormalnystagmus. 9. Muscletoneandmusclemassarenormal. 10. Nosignsofcervicaldiscomfort. 11. Noareasofhyperesthesiaduringpalpationofthevertebralcolumn.
The lesion is in the right cerebellum. The dog has paradoxical vestibular syndrome, a syndrome in which the head tilt and loss of balance are directed towards the side opposite to a central nervous system lesion. This involves the cortex of the folia of the cerebellum at the flocculus and nodulus and/or the caudal cerebellar peduncle. If there is a lesion in the right cerebellum at the flocculus and nodulus and/or at the caudal cerebellar peduncle, there will be a lack of inhibition by the Purkinje cells to the right vestibular nuclei, resulting in excessive discharge of the right vestibular system neurons. In this particular case, the vestibular system with the least activity is the left one. As a consequence of this, the head tilt and loss of balance will be to the left, despite the fact that the true lesion is in the right cerebellum. If a complete neurological examination is carried out, it will be noted that the postural reaction deficits will be in the right fore‐ and hindlimbs, ipsilaterally to the central nervous system lesion. This is because the lesion in the right cerebellum has also interfered with the sensory system that detects position and movement in muscles and joints. MRI scans of the dog’s brain revealed a mass‐like lesion (a suspected primary brain neoplasm) affecting the cerebellar cortex of the right paramedian lobule and flocculus, the right caudal cerebellar peduncle, the nodulus and part of the vermis.
33
A 15‐month‐old Cavalier King Charles Spaniel: 1. Mildataxiainallfourlimbs 2. Muscletonenormal 3. Allspinalreflexesintact 4. Nointentiontremor 5. Occasionalfranticscratchingofneckwithhindpaws
The mild ataxia in this case was hardly noticeable when the dog was walking or running. However, hemiwalking and wheelbarrow testing did reveal the mild abnormality. There was no intention tremor, so it was unlikely that the cerebellum was involved. This suggested that the lesion was affecting the proprioceptive pathways in the spinal cord. Muscle tone was normal so that a UMN lesion was unlikely and normal spinal reflexes indicated that the spinal nerve outflow to the brachial and lumbosacral plexuses were not affected, i.e. no LMN lesion. The neck scratching suggested that an abnormal sensation (possibly pain) was present in the neck. No skin lesion was present so a neuropathic origin of the sensation was possible. A MRI scan of the brain and cervical spine was carried out; this revealed a syrinx in the spinal cord at C2/C3. On transverse scans the syrinx was seen to be located dorsally and was mainly affecting the tracts in the dorsal funiculi. Syringomyelia is a frequent condition in Cavalier King Charles Spaniels and occurs in several other breeds. It is usually associated with an abnormality of the foramen magnum (Chiari‐like malformation)
34
A female yearling lamb: 1. Circlingtotheleft 2. Headavertedtotheleft 3. Ptosis(droopinguppereyelid)andlossoffacialmuscletoneontheleft 4. Dribblingofsalivaontheleft 5. Becamerecumbentwithin3days 6. Mild pyrexia 7. Died7daysafteronset
This lamb was compulsively circling to the left, an abnormal behaviour characteristically due to a lesion in the left cerebral cortex. There was aversion of the head towards the left (i.e. the head rotated with the left ear lower than the right and the nose directed to the right) again suggesting a left cerebral lesion. These signs are typically those of a Coenurus cyst, but a facial paralysis (ptosis and salivation) is not normally found in coenuriasis. No pyrexia occurs in coenuriasis, recumbency does not occur for several weeks and death is not sudden. The clinical signs in this case are typical of inflammation of the brain (encephalitis) due to infection with Listeria
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A 12‐week‐old Chihuahua puppy: 1. Dullanddrowsy 2. Underweight 3. Clumsyandpoormuscletone 4. Lateralstrabismusofbotheyes
This is the typical presentation of a puppy with congenital hydrocephalus. The strabismus may be lateral and/or ventral (‘setting sun sign’) and is most likely due to the skull malformation. The expansion of the lateral ventricles results in loss of cerebral tissue. As a consequence, there are alterations in awareness, consciousness and behaviour. In addition, seizures, paresis, circling and visual deficits may occur. Congenital hydrocephalus occurs in the Chi‐hua‐hua, Pekingese, Yorkshire Terrier, Pug and several other small breeds. Widely open fontanelles are usually found in affected dogs.
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A 12‐month‐old male Border Collie: 1. Threeseizuresatweeklyintervals 2. Theseizureslastedforabout2minutesandwerefollowedbydrowsiness for about 1 hour 3. Theseizuresweretypicalgrandmalfitswithtonic/clonicactivityofthe limbs and salivation 4. Betweentheseizureepisodes,thedogwasapparentlynormal 5. Whenexaminednoneurologicalabnormalitiesweredetected
The Border Collie is one of several breeds of dog that has a high incidence of so‐called idiopathic epilepsy. In this breed and the Keeshond, Golden Retriever, Shetland Sheepdog and German Shepherd, an inherited basis has been identified. Epilepsy is defined as a condition of recurrent seizures. Typically, the seizures commence at 1 to 3 years of age and occur with regularity every few days or weeks. The clinical signs include a brief loss of consciousness and rapid involuntary movements of the limbs. Salivation, urination and defaecation are frequent autonomic signs. Seizures are the manifestation of excessive excitation of the neurons of the cerebral cortex
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An 8‐year‐old male German Shepherd dog: 1. Anataxicgaitofthehindlimbshaddevelopedovertheprevious12 months 2. Deficitsingeneralproprioceptionwerefoundinbothhindlimbs,butnot in the forelimbs 3. Adegreeofhypertoniawaspresentinthemusculatureofthehindlimbs, but not in the forelimbs 4. Thehypertoniadetectedintheearlystagesofthediseasegradually changed to hypotonia and the hindlimb muscles became flaccid 5. Bothdeepandmildpaininthehindlimbswasmaintained 6. Urinationanddefaecationwerenotaffected
The early signs in this patient were ataxia of the hindlimbs and knuckling of the hindpaws, easily recognised by the scraping of the nails; these signs indicate a disturbance of proprioceptive function. This patient was initially hypertonic in the hindlimb muscles and the withdrawal reflexes were exaggerated, suggesting an upper motor neuron lesion. As the condition progressed, the UMN signs changed to LMN indications (hypotonia and depressed reflexes). The clinical signs suggested that the lesion was localised to the spinal cord between the nerve outflows to the brachial and lumbosacral plexuses. The more heavily myelinated pathways were affected first, indicating that the pathogenesis involved early demyelination. This patient was suffering from a degenerative myelopathy. This condition has a high incidence in the German Shepherd Dog and typically shows onset at 6–9 years of age. The change in muscle tone was due to the progressive degeneration of the myelin in the peripheral nerves. The preservation of deep pain and autonomic functions is due to the prevalence of unmyelinated fibres in these pathways.
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A 3‐month‐old Boxer puppy: 1. Progressivehindlimbataxiaandhypermetria(high‐steppinggait) 2. Absentpatellarreflexes 3. Decreasedmuscletoneinallfourlimbs 4. Painsensationintact 5. Electrodiagnostictestinggavepositivesharpwavesandfibrillation potentials together with reduced nerve conduction velocity
This young Boxer puppy showed a severe and progressive hindlimb ataxia with hypermetria (high‐stepping). A lower motor neuron distribution was evident from the depressed spinal reflexes and the lack of muscle tone. Pain perception was maintained. These clinical signs indicated widespread demyelination. Electrodiagnostic testing would reveal positive sharp waves and reduced nerve conduction velocity confirming demyelination and suggesting axon degeneration. Progressive axonopathy is an inherited condition of the Boxer breed and invariably leads to euthanasia.
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A 12‐month‐old Toy Poodle: 1. Acuteonsetofneckpain 2. Tetraparesis/ataxia 3. Wheelbarrow and hemiwalking tests revealed proprioception deficits in all four legs 4. Amildincreaseinmuscletoneinthelimbs 5. Spinalreflexeswerepresentinallfourlimbs
The tetraparesis, ataxia and proprioception deficits affecting all four limbs are consistent with a cervical spinal cord lesion. Both sides are affected, indicating that the lesion is midline or bilateral. The increase in muscle tone in the limbs suggests the presence of an UMN lesion, i.e. in the brain or cervical spinal cord. The presence of neck pain further localises the lesion to the cervical spinal cord. Careful palpation should further localise the lesion to the cranial region of the neck. The diagnosis is likely to be an atlantoaxial subluxation, a dorsal displacement of the cranial body of the axis into the vertebral canal. This subluxation can occur when the dens is absent, as in seen in the toy breeds.
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A litter of five 10‐week‐old kittens: 1. Allthekittenswereapparentlynormalatbirth 2. Theyseemedclumsywhenmovingat5weeksofage 3. Astheybecamemoreambulatory,theydevelopedahigh‐steppinggait (hypermetria) 4. Theyshowedanintentiontremorwhenattemptingtolapfromasaucer 5. Theabnormalmovementswerenon‐progressiveby10weeksofage 6. Thereweredifferencesinthedegreetowhichindividualswereaffected
This a transmissible congenital disease caused by a virus, which has a predilection for the actively dividing cells of the cerebellum. The clinical signs are typical of an extensive cerebellar lesion. Hypermetria and intention tremor are seen frequently when a lesion involves the cerebellum. Once the cerebellum has finished its growth phase, the disease does not progress further but neither does the affected cat show any resolution.