Hypothyroidism endocrine disease that can be reason for very different neurological signs, varying from signs of polyradiculoneuritis to neurological signs from the brain and vestibular disorder.
The good news are that all of this neurological problems and deficits can be reverse with adequate treatment, good nursing and physiotherapy.
I will present 2 cases of hypothyroidism in dogs with very different neurological signs. In first case I did not believe that this disease can manifest so heavy clinical signs. In second case, I took blood sample for fT4 just to be sure that this is not hypothyroidism.
Signalment: Dog, F, 9 y.o., Samoyed
History: Two days ago while the dog is on a walk, the owner noticed small paresis with front legs but it was for few minutes and they went back home. The dog came in the clinic on 1st of December in lateral recumbency, not able to stand up and not able to stay on her legs, even with help. The dog could not eat without help and holding the head and the body.
General examination: no abnormalities, the dog was not vaccinated the last year. Orthopedic examination: no abnormalities.
-Hands off exam:
- Consciousness – normal
- Behavior – can’t find any abnormalities in this position
- Seizers – no seizers
- Body posture – lateral recumbency but the dog can move head and neck
- Gait – symmetrical tetraplegia
-Hands on exam:
- Cranial nerves – no neurological deficits
- Postural reaction – can’t be checked in this position
- Spinal reflexes – absent withdrawal reflex on both front legs, reduced extensor carpi radialis on the right front leg, there are no abnormalities in hind limbs spinal reflexes. Normal tail movement, there is a perineal reflex and normal deep pain sensation.
Localization: C6 – Th2
Differential diagnosis: Degenerative/Neoplastic/Vascular
At this point we were unable to make CT or MRI and the decision was to use steroids in dose 2 mg/kg, famotidine 0,5 mg/kg/12 h p.o., Omeprazole 1 mg/kg/24 h p.o. and to see what will happen on the next day. On the next day the dog was in the same condition and I repeat the steroid. After second injection the dog has profuse diarrhea so we stopped the steroid and treated the GI signs.
Two days later we made CT and there are no abnormalities.
On the next day was taken blood sample for biochemistry and fT4. The biochemistry showed no specific abnormalities, but fT4 was very low.
fT4 – 0,1 pmol/L (7,7 – 47,60 pmol/L)
Creatinin – 39 mmol/L (44,3 – 138,4 mmol/L)
Glucose – 6,2 mmol/L (3,4 – 6,00 mmol/L)
Creatin kinase – 298,1 U/L (13,7 – 119,7 U/L)
LDH – 576,9 U/L (24,1 – 219,2 U/L)
Magnesium – 2,00 mmol/L (0,7 – 1,1 mmol/L)
The algorithm was to start levothyroxine and if we don’t have any results may be the reason for this condition is polyradiculoneurtis.
I didn’t believe that the reason for so hard clinical signs is only hypothyroidism.
Eight days later the dog was with total areflexion of all four limbs.
The decision was to take CSF, muscle biopsy (from M. gastrocnemius, M. triceps brachii) and nerve biopsy (from n. peroneus). The samples (the biopsies and the CSF smear) were send to Laboklin Germany. The cells count, protein, glucose and microbiology of CSF were made in laboratory department of “Dobro hrumvane!” veterinary clinics.
The results were:
Number of cells – normal (<5)
Protein total – 2.4 (<25)
Glucose – 4.6 (80% of normal blood values)
Microbiology – negative
“The smears were cell free. Only few keratin flakes were present.
– striated muscle with multifocal mild degenerative and regeneative
– mild multifocal purulent perivasculitis (M. gastrocnemius)
– histologically normal nervous tissue
Mild multifocal degenerative and regenerative changes of the striated muscle was found. A specific cause was not detected. It should be kept in mind, that in muscle pathology there may not be a strong correlation between histological changes and severity of the clinical symptoms.
Considering the purulent perivasculitis in the sample of the M.
gastrocnemius an inflammatory (possibly infectious) process in other
locations should be excluded clinically.
Signs for a polyneuritis have not been observed within the examined
I had to resign that the most likely cause of Scarlett’s condition was hypothyroidism and we started physiotherapy procedures.
Meanwhile, the patient’s condition has begun to improve. First Scarlett started to move her head better, started to lay on her chest and started eating by herself. The muscle tone start to improve.
40 days later
The day that Scarlett left the clinic.
Signalment: Dog, F, 5 y.o., German shepherd dog
History: Everything started with variable appetite. The dog came in the clinic for second opinion on 06.06.2019.
Colleague already took blood samples and there were no specific abnormalities.
-Hands off exam:
- Consciousness – abnormal
- Behavior – abnormal
- Seizers – no seizers
- Body posture – abnormal, head tilt, from time to time head turn, opisthotonus
- Gait – abnormal, symmetrical, general proprioceptive ataxia
-Hands on exam:
- Cranial nerves – vision, oculovestibular and menace is absent, contraction of the pupils is normal but dilatation is reduced, increased jaw tone, reduced gag reflex and reaction of the tongue.
- Postural reaction – proprioception and hopping are absent
- Spinal reflexes – absent withdrawal reflex on the left front legs, reduced on the right front leg.
Localization: Central vestibular
Differential diagnosis: Metabolic/Inflammatory/Neoplastic
I took blood samples to examine fT4 just to be sure that this is not hypothyroidism.
We discussed with the owner that if there is no abnormalities in thyroid hormones we will take and make some tests with CSF.
The level of fT4 was 1,60 pmol/ L (7,7 – 47,60 pmol/L)L
I started levothyroxine and after two intakes of the medication the result was:
The next few weeks the dog was not still in perfect condition, but there was improvement.
Conclusion: Hypothyroidism is often over diagnosed condition, but is also misdiagnosed metabolic disease with lots of different signs and different manifestation in every part in veterinary medicine.