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Neurology 1 Scientific Proceedings: Companion Animals Programme A simple approach to the neurological examination - brain, brainstem and cerebellum Mette Berendt, DVM, Ph.D., Associate Professor, Dep. of Small Animal Clinical Sciences - Faculty of Life Sciences, University of Copenhagen, DK, Mette Berendt [email protected] Introduction The primary goal of the neurological examination is to identify abnormal clinical neurological signs that may help to identify lesions in the central nervous system (CNS). The clinical signs of neurological dysfunction act as markers for the CNS lesion, and are thus used to establish the neuro-anatomical localisation. Signs of thalamo-cortical dysfunction • Behavioural changes (loosing housetraining, depression, apathy, difficulties recognizing the owner) • Seizures • Abnormal posture (circling in large circles, head pressing) • Visual deficits (central blindness with preserved pupillary reflexes) • Postural/proprioceptive deficits (contra lateral) • Sensibility deficits (contra lateral) Signs of hypothalamic dysfunction • Behavioural changes (disorientation, aggression, hyper excitability, pacing, shaking, hiding) • Abnormal appetite • Abnormal temperature regulation • Signs from hormonal systems Signs of brainstem (formatio reticularis - pons and medulla oblongata - fasciculus longitudinalis medialis) dysfunction Formatio reticularis (situated caudally in the brainstem) holds the ARAS (the ascending reticular activating system). The ARAS is essential for arousal of the cerebral cortex by acting as an impulse generating pacemaker • The ARAS acts upon stimuli such as light, sounds, visual input and movements. Signs of formatio reticularis dysfunction: • Changes in consciousness (somnolence, less playful, lethargy, stupor, coma) The nuclei of cranial nerve III-XII is situated in the pons and the medulla oblongata. Deficits in cranial nerve reflexes/reactions reflect lesions in the peripheral nerve or in the pons/brainstem and are of the most important localising value. 150 | Abstracts European Veterinary Conference Voorjaarsdagen 2008 Signs of pons and medulla oblongata dysfunction: • Cranial nerve deficits (III-XII) The vestibular system (cranial nerve VIII) communicates with the cranial nerve nuclei of III, IV and VI (eye movements) through the Fasciculus Longitudinalis Medialis sitting in the core of the brainstem. • This structure must be intact in order to induce physiological nystagmus Signs of central vestibular system dysfunction Lesions of the central vestibular system arise from the vestibular nuclei situated in the brainstem (central vestibular syndrome). Dysfunction of the vestibular system is characterised by balance problems and asymmetrical ataxia (vestibular ataxia). Other signs of vestibular dysfunction are: • Head tilt (as a rule towards the lesion) • Pathological nystagmus (the fast phase is opposite to the side of the lesion) • Circling (small circles) • Rolling • Vestibular strabismus (ventral deviation of the eye ipsi-lateral to the lesion) Central vestibular syndrome If one or more of the above signs are combined with ipsi-lateral deficits of proprioception and/or signs of dysfunction of the reticular activating system or other cranial nerves than VIII, it is an indication of a central vestibular lesion. Note however, that deficits of CN VII (fascialis) and Horners syndrome may also be present with lesions of the peripheral vestibular system (since these structures are anatomically travelling peripherally closely to the middle ear. They may therefore be affected with e.g. infection or neoplasm of the middle ear). Signs of dysfunction of the cerebellum The cerebellum acts as a coordinator and regulator of motor activity (whereas the motor cortex of the cerebrum initiates movements). The cerebellum controls the speed, direction and force of movement. The cerebellum regulates equilibrium and tonus and thereby supports a normal positioning of the body. Dysfunction of the cerebellum is characterised by one or more of the following signs: • Incoordination and dysmetria (most often hypermetria) Neurology Scientific Proceedings: Companion Animals Programme • • • • with preserved strength- so called cerebellar ataxia. Spasticity (hypertonia) Head (and maybe body) tremor Lack of menace response Vestibular signs (if lesions of lobus flocculonodularis are present) Signs of dysfunction of ascending proprioceptive and postural pathways travelling from the peripheral receptors through the spinal chord to the cerebral cortex and descending Upper Motor Neuron (UMN) pathways arising in the cerebral motor cortex interacting with the Lower Motor Neurons (LMN) through the spinal chord • Lesions of the above pathways in the thalamus, capsula interna or cortex are reflected clinically as contra lateral deficits, whereas lesions caudally to the thalamus (the pathways crosses the midline here) will be reflected clinically as ipsi-lateral deficits References 1. De Lahunta A. Veterinary neuroanatomy and clinical neurology. Philadelphia, WB Saunders 1983;p.365-387. 2. Braund KG. Clinical syndromes in veterinary neurology, 2.ed. Missoury, Mosby 1994;p.1-36 3. Clinical Neurology in Small Animals - Localization, diagnosis and treatment. Ed. Braund K & Vite C. www.ivis.org International Veterinary Information Service, Cornell University, NY, USA, 2005. Abstracts European Veterinary Conference Voorjaarsdagen 2008 | 151 1