A 13-year-old, female, spayed, domestic shorthair cat was referred to the neurology service of the Small Animal Clinic at the University of Berne (Switzerland) with a history of behavioral changes for the past 10 days. According to the owner, the cat seemed to be mostly apathetic but occasionally attacked objects and displayed bizarre playing behavior. She was also reluctant to jump on furniture or to walk over obstacles and did not recognize her sleeping places anymore. In addition, the cat showed intermittent compulsive walking and refused to eat dry food. Before being referred to our clinic, the cat was treated with carprofen (2 mg/kg PO q24h) for 5 days, with no effect.The clinical examination of the cat revealed a poor body condition and obesity. The heart and respiration rates, as well as the body temperature, were within normal limits. The cat was apathetic and disorientated. The cat's aggressive behavior was striking, seemingly without reason. Head and neck postures were very rigid, and the cat reacted aggressively when manipulated. The gait was characterized by a generalized sensory ataxia, with a tendency for compulsive walking. There were slight proprioceptive deficits of the left hind and front limbs. The menace response on the left side was slightly decreased. The cervical vertebral column appeared painful on palpation. The neurologic findings suggested a localization in the right forebrain.Results of a CBC were within normal values. Serum biochemistry results revealed a slightly increased total protein concentration (8.9 g/dL; reference range, 5.6-7.8 g/dL) and a fasted cholesterol serum concentration at the upper limit, with 175 mg/dL (reference range, 64-229 mg/dL). The erythrocyte sedimentation rate was increased, at 13 mm after 1 hour (reference range, 0-2 mm) and 41 mm after 2 hours (reference range, 2-10 mm). The urine pH was 7.4 (reference range, pH 5-7), with trace protein but no other abnormalities. Feline leukemia virus and feline immunodeficiency virus tests were both negative.Cerebrospinal fluid revealed a negative Pandy's test, 21 cells/mL and 30 mg/dL albumin. The differential cell count revealed 80% lymphocytes, 15% monocytes, and 5% macrophages.Magnetic resonance imaging (MRI) of the brain was performed with a 0.3 Tesla MRI unit.a Sequences included a fast spin echo (FSE) T2 in sagittal and transverse orientation, a field echo (FE) T2 a and a FE three dimensional (3D) T1 in transverse plane; a fluid attenuating inversion recovery (FLAIR) cerebrospinal fluid (CSF-suppression), a short tau inversion recovery (STIR) (fat-suppression), and a FE 3D multiplanar reconstruction (MPR) (high resolution T1w gradient echo) in the dorsal plane. After IV injection of 0.15 mmol gadodiamide b ), the T1-weighted sequences were repeated. The MRI showed an extensive spaceoccupying lesion in the area of the falx cerebri, which reached from the olfactory bulbs to the tentorium cerebelli. It compressed both hemispheres and deformed the third and the lateral ventricles, as well as the thalamus. The lesion...

We report a congenital follicular dysplasia in five coatis from four different litters of the same parents born between 1996 and 2001. These coatis were born apparently alopecic with the entire body covered by very short dark hairs, with secondary lichenification of the skin, crusting and scaling. The main histopathological feature consisted of premature cornification of the cortical cells of the hair shaft. Cells were already fully cornified below the Adamson's fringe, leading to a disorganized, fragmented and constricted hair shaft. Based on the history of the animals and the nature of the lesions, a genetic defect in hair shaft keratinization was suspected.

A 13-year-old, female, spayed, domestic shorthair cat was referred to the neurology service of the Small Animal Clinic at the University of Berne (Switzerland) with a history of behavioral changes for the past 10 days. According to the owner, the cat seemed to be mostly apathetic but occasionally attacked objects and displayed bizarre playing behavior. She was also reluctant to jump on furniture or to walk over obstacles and did not recognize her sleeping places anymore. In addition, the cat showed intermittent compulsive walking and refused to eat dry food. Before being referred to our clinic, the cat was treated with carprofen (2 mg/kg PO q24h) for 5 days, with no effect.The clinical examination of the cat revealed a poor body condition and obesity. The heart and respiration rates, as well as the body temperature, were within normal limits. The cat was apathetic and disorientated. The cat's aggressive behavior was striking, seemingly without reason. Head and neck postures were very rigid, and the cat reacted aggressively when manipulated. The gait was characterized by a generalized sensory ataxia, with a tendency for compulsive walking. There were slight proprioceptive deficits of the left hind and front limbs. The menace response on the left side was slightly decreased. The cervical vertebral column appeared painful on palpation. The neurologic findings suggested a localization in the right forebrain.Results of a CBC were within normal values. Serum biochemistry results revealed a slightly increased total protein concentration (8.9 g/dL; reference range, 5.6-7.8 g/dL) and a fasted cholesterol serum concentration at the upper limit, with 175 mg/dL (reference range, 64-229 mg/dL). The erythrocyte sedimentation rate was increased, at 13 mm after 1 hour (reference range, 0-2 mm) and 41 mm after 2 hours (reference range, 2-10 mm). The urine pH was 7.4 (reference range, pH 5-7), with trace protein but no other abnormalities. Feline leukemia virus and feline immunodeficiency virus tests were both negative.Cerebrospinal fluid revealed a negative Pandy's test, 21 cells/mL and 30 mg/dL albumin. The differential cell count revealed 80% lymphocytes, 15% monocytes, and 5% macrophages.Magnetic resonance imaging (MRI) of the brain was performed with a 0.3 Tesla MRI unit.a Sequences included a fast spin echo (FSE) T2 in sagittal and transverse orientation, a field echo (FE) T2 a and a FE three dimensional (3D) T1 in transverse plane; a fluid attenuating inversion recovery (FLAIR) cerebrospinal fluid (CSF-suppression), a short tau inversion recovery (STIR) (fat-suppression), and a FE 3D multiplanar reconstruction (MPR) (high resolution T1w gradient echo) in the dorsal plane. After IV injection of 0.15 mmol gadodiamide b ), the T1-weighted sequences were repeated. The MRI showed an extensive spaceoccupying lesion in the area of the falx cerebri, which reached from the olfactory bulbs to the tentorium cerebelli. It compressed both hemispheres and deformed the third and the lateral ventricles, as well as the thalamus. The lesion...