Download a simple approach to the neurological

Neurology
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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.
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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
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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.
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