DeLahunta Chapter 13 - Cerebellum Flashcards
Up until which day during gestation, the formation of Purkinje neurons is
completed in calf?
100d of gestation
Which are the two regions of the cerebellum, and what is separating them?
The cerebellum is divided into two disproportionate regions: (1) the large body of the cerebellum and (2) the small flocculonodular lobe. These two regions are separated by the uvulonodular fissure
Please name the cells, fibres and layers of the cerebellum.
Layers (external to internal):
-molecular
-purkinje
-granular
then nuclei within white matter: FID (fastigial, interposital, dentate)
Fibers are:
mossy (coming from brainstem/spinal cord) and they synapse with cerebellar nuclei and granule cells
climbing fibers (coming from olivary nucleus) and synpase some with cerebellar nuclei and some are climbing to the purkinje vertical axons within the molecular
Which is the ONLY neuron of cerebellar cortex that projects to the medulla of cerebellum?
Purkinje cell to the cerebellar nuclei (most of them - inhibitiory - GABA)
and some to vestibular nuclei (through floculonodular lobe) (inhibitory, GABA)
Which neurotransmitter is released at the synapse of the mossy fibres and which
one at the synapse of the climbing fibres? Which neurostramitter is released at
the synapse between granule cells and Purkinje neurons? What is the function of
the neurotrnsmitters?
Mossy fibers (cells) to granule cells–> ACH (+)
Climbing fibers (cells) to Purkinje–> ASPARTATE (+)
Granule cells to Purkinje cells (in the mollecular layer) –> GLUTAMATE (+)
Stelate (in mocelucar but also in granular layer) to both purkinje and granule–>INHIBITORY
Purkince to cerebellar nuclei + vestibular nuclei (through floculonnodular lobe) –> INHIBITORY (GABA)
Where are the cerebellar nuclei sending effrents to and via which peduncle?
1) direct from purkinje cells (via floculonodular lobe) to the vestiular nuclei (CAUDAL cerebellar peduncle)
2) fastigial n. –> vestibular nuclei + ARAS (CAUDAL CP)
3) interposital n. –> red nucleus + ARAS (ROSTRAL CP)
4) dentate n. –> red nucleus + ARAS + Pallidum + ventral lateral thalami nucleus (ROSTRAL CP)
The 3 and 4 CROSS in the ventral tegmental decusaion (caudal colliculi) –.> contratlateral
Please give example of viruses responsible for cerebellar hypoplasia in dog, cat, calf, pig, human
dog - Herpes virus,
cat -parvoviral infection,
calf - bovine viral diarrhoea,
pig- swine fever,
human -zika virus
Which cerebellar layer is at risk in cats with feline panleukopenia virus? What is the consequence of this?
External germinal layer, distruction of this prevents the formation of the granular layer – hence name granulopival hypoplasia
Which are the clinical signs of arabian foals with abiotrophy? At which age are the
clinical signs noticed? Which gene is responsible Brault et al.,2011?A head
A head and neck tremor may be the earliest clinical sign observed. Owners often report that when they are halter training the foal its head bobs, and with little stimulation, the foal will rear up, lose its balance, and fall over backward. Although the gait may somewhat mimic a UMN and GP system dysfunction in the cervical spinal cord, the intentional head tremor and the tendency to rear up with the thoracic limbs in full extension when stimulated excludes this consideration. In addition, horses with this cerebellar cortical abiotrophy lose their menace response. From birth, to a few months of age
gene: MUTAH gene
Based on a Study by Fisher et al., a) which were the most common neurological signs secondary to infection with Neospora caninum? b) most common neuroanaotmicla locliastion
c)Following treatment, what
was the relapse rate?
d) What was the complete improvement rate?
a) Cerebello-vestibular signs predominated; however, presenting clinical signs were varied and the neurolocalisation was often
b) multifocal in nature (46.3%), making neosporosis an important differential diagnosis for meningoencephalitis of unknown origin.
d) Complete clinical improvement was rare (5.6%),
c) and relapses were common (27.8% cases with follow-up).
Which plant may cause cerebellar cortical degenration in cattle (https://www.sciencedirect.com/science/article/abs/pii/S1090023309001531#fig2) ?
Solanum kwebense
What clinical signs may you see with a lesion to the rostral lobe of the cerebellum and why?
is especially inhibitory to the stretch reflex mechanism of antigravity muscles (extensor muscle tone). Lesions in this area may result in opisthotonus with rigidly extended thoracic limbs. In some instances, the pelvic limbs may be flexed cranially ventral to the trunk, by hypertonia of the hypaxial muscles that flex the hips. The combination of extended neck and thoracic limbs with flexed hips is called a decerebellate posture.
Name the breed affected by a specific hereditary ataxia deemed a form of spinocerebellar degeneration. How may these dogs present and what gene has been identified?
Jack/Parson Russell and Smooth Fox Terriers
The onset of the clinical signs varies from 2 to 9 months of age and usually starts in the pelvic limbs and progresses to the thoracic limbs. After several months of slow progression, the disease may become static. We have seen dogs 10 to 12 years old with these clinical signs unchanged since 1 to 2 years of age.
Mutation in KCNJ10 that encodes a glial potassium channel that regulates neuronal excitability.
Which 2 breeds have been described with cerebellar abiotrophy with degenerative lesions also in extrapyramidal nuclei? Which gene has been identified?
Kerry Blue Terrier and Chinese Crested breeds
Mutation has been identified in the SERACI gene for this disorder.
Name 3 breeds in which a late-onset cerebellar cortical abiotrophy has been recognized:
Name the genes for 2 of them.
Gordon Setter, Old English Sheepdog, American Staffordshire Terrier and Brittany Spaniel, Lab
Gordon setter-Old english: RAB24 gene
