Cerebellar hypoplasia (CH) is a neurological condition in which the cerebellum is smaller than usual or not completely developed.[1] It has been reported in many animal species.[2]
The cerebellum is the brain's main control center for planning, adjusting, and executing movements of the body, the limbs and the eyes. It plays a major role in several forms of motor learning, including balance and posture.[3]
In the past, the evidence for a role for the cerebellum in cognitive functions was rather weak.[4] However, investigations into the cognitive neuroscience of the cerebellum are rapidly advancing, extending far beyond the traditional view. For humans, current theories support that what the cerebellum does to sensorimotor and vestibular control, it also does to cognition, emotion, and autonomic function.[5][6] How it functions in cognition, emotion, or autonomic function in animals is still largely unknown. In 2012, a study in mice provided direct evidence that subtle disruptions in cerebellar architecture can have pronounced effects on behaviors typically associated with autistic-like behavior.[7]
Development of the cerebellum starts in a fetus in utero and, depending on the species, may continue for some period after birth. Postnatal development periods vary by species including: dogs up to 75 days, cats to 84 days, calves up to six months.[8]
A hereditary link to CH has been established in some animals, including certain breeds of cows[2] and dogs.[9]
There are numerous other potential causes for CH. It is suspected that the most common cause is animal parvoviruses.[10]
Feline panleukopenia ("FPLV" a.k.a. Feline Distemper or Feline Parvo) virus has long been known to cause cerebellar hypoplasia in neonatal kittens through in utero or perinatal infection.[11] In utero, the virus can pass from the dam to the developing fetus and may then disrupt the development of its cerebellum by hindering cell division. This can happen when the dam is actively infected with the virus or given a modified-live FPV vaccine when pregnant.[12] Kittens are particularly vulnerable to CH, in particular when the protective antibodies present in their mothers' milk are no longer present at four to twelve weeks of age. Unvaccinated adult cats are also prone to developing the condition.[13]
In most cases the cause is unknown. However, in dogs and cats it is thought to be most likely related to in utero viral infections, toxins or genetic disorders.[14]
Other possible causes, if they occurred during the development period of the cerebellum and inhibit its growth, include:[15]
Numerous problems can be mistaken for CH. These include (but are not limited to):
In 2004, a study was published that linked ketamine to post-anesthetic cerebellar dysfunction in cats.[20] 11 cats that did not have any indication of cerebellar deficits before surgery developed deficits post-surgery. All of these cats were Persian crossbreeds. Ketamine can cause erratic and spastic, jerky movements and muscle tremors and is slow to be metabolized out of the system.[citation needed] The 2018 American Association of Feline Practitioner's Feline Anesthesia Guidelines[21] lists numerous alternatives. Gas anesthesia offers a number of advantages in many circumstances. In CH cats the rapid recovery is its primary advantage.[citation needed]
If the root cause of the CH impacted other parts of the developing brain and/or body, the overall health and life-span may or may not be impacted. For instance, fetuses infected in utero by FPLV that survive, and kittens less than a few weeks of age that become infected with it, can also have retinal dysplasia, and optic neuropathy.[22]