scott@vtx-cpd.com

Replying to Jo T. 29/07/2025 - 21:57

Thanks Jo.

Really interesting case! Would love to here how things progress.

Keep us posted. I hope you are having a good week.

Scott 🙂

Replying to Josep B. 26/07/2025 - 02:38

Thanks Josep.

This is really interesting. Thank you for sharing your thoughts.

Scott 🙂

Hi Jo,

Thanks for sharing this case. This is a tricky one!

1. Could untreated paroxysmal dyskinesia (PD) cause the PU/PD or the high sodium?

Paroxysmal dyskinesia itself doesn’t have a known causal link to hypernatremia or PU/PD. It is a movement disorder without established systemic or metabolic sequelae. However, if the episodes are prolonged or more frequent than recognised, one theoretical possibility is that excessive panting during or after episodes could contribute to insensible water loss, although this would typically lead to free water depletion rather than sodium gain — and would not explain persistent isosthenuria or the absence of compensatory polydipsia unless there’s impaired thirst (see below).

So, while PD is very unlikely to be the primary driver, it’s still important to ensure the dyskinesia isn’t masking other neurologic signs that could indicate central causes of thirst or ADH dysregulation.

2. Could this be primary diabetes insipidus (DI)?

Yes, central DI (CDI) remains a plausible differential, particularly given:

Hypernatremia (Na = 170)

Isosthenuria (USG 1.010)

A clinically well dog with minimal systemic signs

That said, I’d add that in patients with psychogenic polydipsia or diabetes insipidus, the PU/PD that owners observe is often quite dramatic, so I would be a bit surprised if this had gone unnoticed, even in a multi-dog household. If they haven’t seen obvious polyuria or polydipsia, I’d lean more toward intermittent leakage or a true storage disorder as the more likely cause of the nocturnal incontinence.

That being said, I do think it’s worth ruling out other causes of PU/PD as comprehensively as possible before committing to a diagnosis of urethral sphincter mechanism incompetence (USMI) alone. Specifically:

Check ionized calcium

Perform an abdominal ultrasound (both for kidneys and adrenals)

Review diet and treats (for salt intake)

Consider a desmopressin trial over a water deprivation test, I agree that a WDT wouldn’t be indicated here given the current hypernatremia

If there’s any suggestion of CDI or hypodipsia, a trial of DDAVP (desmopressin) is low-risk and diagnostically useful: if the dog concentrates his urine and sodium normalises, that would support central DI. And if there’s leakage at night that persists independently of water balance, then USMI is very likely — and it may have been tipped over the edge by mild underlying polyuria or decreased urethral tone with age.

I’ll double check with our neurologist as well, but I’d say based on the information so far, this sounds more like a storage disorder, and I’d be inclined to continue treatment for incontinence while also covering your bases diagnostically.

3. Could propalin (phenylpropanolamine) affect the paroxysmal dyskinesia?

There’s no strong evidence of an association, but theoretically, as a sympathomimetic, PPA could lower seizure threshold or increase CNS excitability. While PD is not epileptic in nature, there may still be overlap in some patients with idiopathic movement disorders.

If you notice an increase in frequency, duration, or severity of dyskinesia episodes after starting propalin, it would be worth reconsidering. On the other hand, if the incontinence is actually secondary to polyuria, addressing the underlying cause (e.g. DI or CKD) will be more effective than treating the sphincter alone.

Hypernatremia almost always reflects a relative or absolute water deficit, and far less commonly, excess sodium gain. The causes can be grouped as follows:

Pure water loss (e.g. diabetes insipidus, panting, inadequate intake)

Loss of hypotonic fluids (vomiting, diarrhoea, CKD, AKI, diuretics)

Salt intoxication (e.g. homemade playdough ingestion)

Hypodipsia or adipsia (congenital or acquired hypothalamic dysfunction)

Iatrogenic sodium gain (e.g. hypertonic saline, NaHCO₃, high-Na diet)

Endocrine causes (hyperaldosteronism, hypercortisolism — rare to cause frank hypernatremia but do promote sodium retention)

Next steps might include:

Recheck serum sodium and osmolality to confirm degree and trend

Ionised calcium (to exclude hypercalcaemia-driven PU/PD)

Abdominal ultrasound for kidneys, adrenals, and bladder

Desmopressin trial (diagnostic and potentially therapeutic)

Continue PPA trial, with caution and monitoring of PD episodes

Consider MRI or neurologic consult if concern for central hypodipsia emerges

Let me know what you find. Really appreciate you sharing this one!

Have a great weekend.

Scott 🙂

Replying to Jo T. 24/07/2025 - 08:27

Thanks Jo.

So glad it was helpful! Let us know if you have any other questions.

Scott 🙂

Hey Christina!

Thank you for sharing such an interesting case. Definitely one for Liz! I will make sure she sees it.

This sort of case would stress me out!

Scott 🙂