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Arachnoid Cyst/Diverticula
Intracranial
  • Description
  • Signalment
  • Clinical Features
  • Neurolocalization
  • Genetics
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Focal cystic structures involving the components of the meninges are often referred to as arachnoid or subarchnoid cysts. It is debatable whether these abnormalities are present at birth or are acquired during postnatal development.
Age of Onset: Any age of animal can be affected
​
Sex Predisposition: Any sex of animal can be affected
Clinical Course:
Clinical signs may worsen over time
​


Clinical Signs:
Clinical signs of nervous system dysfunction depend on which regions of the nervous system are involved.  

Behavioral/Mental Awareness 
Behavioral changes
Head pressing
Compulsive gait/Circling

Posture and Appearance 
Skin abrasions on the dorsum of thoracic paws
Wide-based stance
Head tilt
Ventrolateral strabismus
Pleurothotonus
Seizures (can be focal or generalized)
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Movement
Falling to the side
Paresis
Head swaying
Ataxia
Hypermetria
Rigid gait
Intention tremor

Proprioception 
Postural reactions delayed in all four limbs

Cranial Nerves 
Menace deficits
Head tilt
Trigeminal nerve deficits (facial hypalgesia, masticatory muscle atrophy)
Facial paralysis


Spinal Reflexes 
Decreased in the thoracic limbs

Special Reflexes (e.g. cutaneous trunci) 
Reduced oculocephalic reflexes
Positional vertical nystagmus

Special Functions (e.g. respiration; urination) 
Central blindness
 
Pain Sensation 
Neck pain

Other
Ventriculomegaly/hydrocephalus​
Typically found in or around the dorsal midbrain, third ventricular region (quadrigeminal cistern), rostral and dorsal to the cerebellum, or at the cerebellopontine angle.
Unknown
To read more about this disease click below:
References
Quadrigeminal/Supracollicular
  • Description
  • Signalment
  • Clinical Features
  • Neurolocalization
  • Genetics
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Quadrigeminal/supracollicular (arachnoid) cysts are abnormal accumulations of cerebrospinal fluid within the arachnoid membrane, associated with the third and/or fourth ventricles, leading to compression of the adjacent parenchyma
Age of Onset: Any age of animal can be affected (mean age of 3 years)
​


Sex Predisposition: Any sex of animal can be affected, although males may be more commonly affected than females
Clinical Course:
Clinical signs may worsen over time
​

Clinical Signs:
Behavioral/Mental Awareness
Seizures (focal or generalized)
Behavioral changes
Compulsive walking
Head pressing

Movement
Ataxia
Hypermetria
Wide-base stance
Intention tremor

Proprioception
Proprioceptive deficits

Cranial Nerves
Menace deficit
Positional nystagmus

Painful Reactions
Cervical hyperesthesia
Intracranial - middle and caudal cranial fossa
Unknown
To read more about this disease click below:
References
Spinal
  • Description
  • Signalment
  • Clinical Features
  • Neurolocalization
  • Genetics
<
>
Spinal arachnoid cysts are reported with increasing frequency in dogs. The term "cyst" is misleading as the tissue bordering the fluid pocket is not lined by a secretory cell layer and there is no epithelial lining to the cyst. A congenital etiology for lesion is suggested, although acquired meningeal inflammation/scarring has been implicated in both human beings and dogs. Scarring of the pia or other meninges may result in the creation of localized CSF accumulation. There is a web-like configuration of aberrant arachnoid and similar tissues that form pockets where CSF can be trapped and accumulated. It is also possible that abnormal cerebrospinal fluid dynamics contribute to cyst formation.  The superficial spinal cord vascular structures are also often abnormal in the region of the cyst and are often prominent at the borders of the abnormality.  Similar to syringomyelia, this spinal cord compression may be dynamic and pulsatile. With situations associated with increases in subarachnoid CSF pressure such as during the Valsalva maneuver, the pressure within this cyst may increase dramatically.

In younger animals, arachnoid cysts may reflect a congenital diverticulum of the subarachnoid space possibly associated with abnormal development of the arachnoid, dural, and pial tissues.
Age of Onset: Onset of clinical signs has been most commonly reported in dogs less than 18 months of age, but any age of animal can be affected.
​
Sex Predisposition: Any sex of animal can be affected
Clinical Course:
​Clinical course is variable from asymptomatic to progressive neurologic deficits
​
Clinical Signs:
Movement
Ataxia
Paresis (in some cases thoracic limbs may be more affected than pelvic limbs)

Proprioception
Proprioceptive deficits

Spinal Reflexes
Hyperreflexia of pelvic limbs
Hypertonicity of pelvic limbs

Special Functions (e.g. respiration; urination)
Fecal incontinence (normal stool in inappropriate locations and without the normal posturing associated with defecation)
**Often dropping feces while walking
​Urinary incontinence


Painful Reactions
​Paraspinal discomfort on palpation
Spinal (Cervical > Thoracolumbar > Lumbar/Caudal)
Unknown
To read more about this disease click below:
References
To read more about this disease click below:
References
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